Science Guardian

Truth, beauty and paradigm power in science and society

I am Nicolaus Copernicus, and I approve of this blog

I am Richard Feynman and I approve of this blog

News, views and reviews measured against professional literature in peer reviewed journals (adjusted for design flaws and bias), well researched books, authoritative encyclopedias (not the bowdlerized Wiki entries on controversial topics) and the investigative reporting and skeptical studies of courageous original thinkers among academics, philosophers, researchers, scholars, authors, and journalists.

Supporting the right of exceptional minds to free speech, publication, media coverage and funding against the crowd prejudice, leadership resistance, monetary influences and internal professional politics of the paradigm wars of cancer, HIV(not)AIDS, evolution, global warming, cosmology, particle physics, macroeconomics, information technology, religions and cults, health, medicine, diet and nutrition.

***************************************************

HONOR ROLL OF SCIENTIFIC TRUTHSEEKERS

Halton C. Arp wki/obit/txt/vds/txt/txt/bk/bk, Henry Bauer txt/blg/ blg/bks/bk/txt/bk/vd, John Beard bk, Harvey Bialy bk/bk/txt/txt/rdo/vd, John Bockris bio/txt/ltr/bk, Donald W. Braben, Peter Breggin ste/fb/col/bks, Darin Brown txt/txt/txt/txt/txt/vd, Giordano Bruno bk/bio/bio, Frank R. Buianouckas, Stanislav Burzynski mov, Erwin Chargaff bio/bk/bio/prs, James Chin bk/vd, Nicolaus Copernicus bk, Mark Craddock, Francis Crick vd, Paul Crutzen, Marie Curie, Rebecca Culshaw txt/bk, Roger Cunningham, Charles Darwin txts/bk, Erasmus Darwin txt//bk/txt/hse/bks, Peter Duesberg ste/ste/bk/txt/vd/vd, Freeman Dyson, Albert Einstein, Richard Feynman bio, John Fewster, Rosalind Franklin, Bernard Forscher tx, Galileo Galilei, Walter Gilbert vd, Goethe bio/bk/bio, Nicolas Gonzalez tlk/rec/stetxt/txt, Alec Gordon, James Hansen, Etienne de Harven bk/txt/vd, Alfred Hassig intw/txt, Robert G. Houston txt, Steven Jonas vd, Edward Jenner txt, Benjamin Jesty, Adrian Kent vd, Thomas Kuhn, Fred Kummerow, Stefan Lanka txt/txt/vd, Serge Lang, John Lauritsen vd, Paul Lauterbur vd, Mark Leggett, Richard Lindzen, James Lovelock, Andrew Maniotis, Lynn Margulis, Barbara McClintock, Christi Meyer vd, George Miklos, Marco Mamone Capria, Peter Medawar, Luc Montagnier txt/txt/vd, Kary Mullis, Linus Pauling prs/vd/vd, Eric Penrose, Roger Penrose vd, Max Planck, Rainer Plaga, David Rasnick /vd, Robert Root-Bernstein vd, Sherwood Rowland, Otto Rossler, Harry Rubin, Marco Ruggiero txt/txt/intw/vd, Bertrand Russell Carl Sagan vd, Erwin Schrodinger, Fred Singer, Barbara Starfield txt, Gordon Stewart txt/txt, Richard Strohman, Thomas Szasz, Nicola Tesla bio/bio, Charles Thomas intw/vd, Frank Tipler, James Watson vd/vd, Alfred Wegener vd, Edward O. Wilson vd.

ACADEMICS, DOCTORS, AUTHORS, REPORTERS AND COMMENTATORS WHO HAVE NOBLY AIDED REVIEW OF THE STATUS QUO

Jad Adams bk, Marci Angell bk/txt/txt/txt, Clark Baker ste/txt/rdo/vd, James Blodgett, Tony Brown vd, Hiram Caton txt/txt/txt/bk/ste, Jonathan Collin ste , Marcus Cohen, David Crowe vd, Margaret Cuomo, Stephen Davis BK/BK,/rdo, Michael Ellner vd, Elizabeth Ely txt/txt/ste, Epicurus, Dean Esmay, Celia Farber bio/txt/txt/txt/vd, Jonathan Fishbein txt/txt/wk, T.C.Fry, Michael Fumento, Max Gerson txt, Charles Geshekter vd, Michael Geiger, Roberto Giraldo, David Healy txt, Bob Herbert, Mike Hersee ste/rdo, Neville Hodgkinson txt /vd, James P. Hogan, Richard Horton bio/vd/vd, Christopher Hitchens, Eric Johnson, Claus Jensen vd, Phillip Johnson, Coleman Jones vds, William Donald Kelley, Ernst T. Krebs Sr txt, Ernst T. Krebs Jr. txt,/bio/txt/txt/ltr, Paul Krugman, Brett Leung MOV/ste/txt/txt/tx+vd/txt, Katie Leishman, Anthony Liversidge blg/intv/intv/txt/txts/txt/intv/txt/vd/vd, Bruce Livesey txt, James W. Loewen, Frank Lusardi, Nathaniel Lehrman vd, Christine Maggiore bk/ste/rec/rdo/vd, Noreen Martin vd, Robert Maver txt/itw, Eric Merola MOV, Lady Mary Wortley Montagu, Michael Moore bio/MOV/MOV/MOV, Gordon Moran, Ralph Nader bk, Ralph Moss txt/blg/ste/bks, Gary Null /txt/rdo/vd, Dan Olmsted wki, Toby Ord vd, Charles Ortleb bk/txt/bk/intw/flm, Neenyah Ostrom bk, Dennis Overbye, Mehmet Dr Oz vd, Eleni Papadopulos-Eleopulos ste/vd, Maria Papagiannidou bk, Thomas Piketty bk/bk/bk/bk/bk/bk/bk/bk/bk/bk, Robert Pollin txt/vd/bk, Jon Rappoport bio/bk/bk/ste/bk/bk/vd, Janine Roberts bk/bk, Luis Sancho vd, Liam Scheff ste/txt/bk/bk/rdio/vd, John Scythes, Casper Schmidt txt/txt, Joan Shenton vd/vd, Joseph Sonnabend vd, John Stauber, David Steele, Joseph Stiglitz bk/txt, Will Storr rdo Wolfgang Streeck, James P. Tankersley ste, Gary Taubes vd, Mwizenge S. Tembo, John Tierney vd, Michael Tracey, Valendar Turner rec, Jesse Ventura bk, Michael Verney-Elliott bio/vds/vd, Voltaire, Walter Wagner, Andrew Weil vd, David Weinberger bio/bk/blg/blg/BK/bk/pds, Robert Willner bk/txt/txt/vd, Howard Zinn.

*****************************************************
I am Albert Einstein, and I heartily approve of this blog, insofar as it seems to believe both in science and the importance of intellectual imagination, uncompromised by out of date emotions such as the impulse toward conventional religious beliefs, national aggression as a part of patriotism, and so on.   As I once remarked, the further the spiritual evolution of mankind advances, the more certain it seems to me that the path to genuine religiosity does not lie through the fear of life, and the fear of death, and blind faith, but through striving after rational knowledge.   Certainly the application of the impulse toward blind faith in science whereby authority is treated as some kind of church is to be deplored.  As I have also said, the only thing that ever interfered with my learning was my education. I am Freeman Dyson, and I approve of this blog, but would warn the author that life as a heretic is a hard one, since the ignorant and the half informed, let alone those who should know better, will automatically trash their betters who try to enlighten them with independent thinking, as I have found to my sorrow in commenting on "global warming" and its cures.
Many people would die rather than think – in fact, they do so. – Bertrand Russell.

The progress of science is strewn, like an ancient desert trail, with the bleached skeletons of discarded theories which once seemed to possess eternal life. - Arthur Koestler

One should as a rule respect public opinion in so far as is necessary to avoid starvation and to keep out of prison. – Bertrand Russell

A sudden bold and unexpected question doth many times surprise a man and lay him open. – Sir Francis Bacon (1561 – 1626)

He who knows only his own side of the case, knows little of that. – John Stuart Mill

No problem can withstand the assault of sustained thinking. – Voltaire

Might the simple maxim, that honesty is the best policy be laid to heart! Might a sense of the true aims of life elevate the tone of politics and trade, till public and private honor become identical! – Margaret Fuller Ossoli

Although science has led to the generally high living standards that most of the industrialized world enjoys today, the astounding discoveries underpinning them were made by a tiny number of courageous, out-of-step, visionary, determined, and passionate scientists working to their own agenda and radically challenging the status quo. – Donald W. Braben

(Click for more Unusual Quotations on Science and Belief)

IMPORTANT: THIS SITE IS BEST VIEWED ONLY IN VERY LARGE FONT
All posts guaranteed fact checked according to reference level cited, typically the original journal studies. Further guide to site purpose, layout and how to print posts out is in the lower blue section at the bottom of the home page.

Misguided Guide May Solve AIDS’s Biggest Problem

Hidden in New Yorker piece, a way of moving on from HIV hysteria

How the top ranks could rationalize flipping reality the right way up again

Can you see it? Hint included

spector.jpgThe unstoppable Michael Specter has produced an update review in the New Yorker of the latest thinking on retroviruses, which makes a number of remarkable but somewhat unconvincing claims, if you know anything about the topic.

It has one point of interest for all paradigm war observers in HIV=AIDS, however, which provides what in our view is the answer to the vexed question all informed supporters and promoters of the paradigm HIV-is-the-cause-of-AIDS secretly worry over, namely, How the heck do we get out of this debacle?

The hippopotamus in the AIDS bath

For any admission of what has really been going on in the past twenty years in HIV=AIDS – possibly over a hundred billion dollars spent, much of it public money, on an absurd, unsubstantiated, self-contradicting paradigm dreamed up by a known rascal and perpetrated by a self serving bureaucrat with the scientific grasp of a gnat on a world he prevents from reviewing it by barring respectable reporters from even mentioning the topic of all the excellent papers in the AIDS literature rejecting the tenets of the overarching but hollow belief.

Papers, that is, written not only by Duesberg but also by none other than Anthony Fauci and our heroic debunker basher John P. “I am not a macaque, but a fine scientist who tests microbicide on the nether regions of macaques” Moore of Weill-Cornell – threatens to bring the grand institutions and great names of science into such disrepute that they will never recover their authority.

Imagine if Science and Nature had to admit a failure of peer review so embarrassing that twenty years of study and discussion are revealed to have been based on a very silly and unjustified belief, one that has led to dosing hundreds of thousands of people – potentially millions – with extremely damaging drugs that have not only failed to rescue patients suffering from other, misattributed, real illnesses but actually hurried them to their graves, patients who have included some of the most important cultural figures in America?

hippounderwater.jpgImagine what effect that would have on public and charitable support and funding of these august institutional and personal pillars of the scientific community, most of which is not to blame for this vast fiasco.

Where would that leave the reputation of the Lasker Awards, who have dispensed more than one prize to those who promote this insupportable distortion of science, though they have not been followed by a prize from the Nobel committee in the usual way, a fact that gives one hope that there are those in Stockholm who are better informed on what is going on, and reluctant to give the greatest accolade to such as Robert Gallo.

After all, a Nobel is meant to recognize good done to humanity, not a self serving claim which has been bolstered by artificial support from a censoring NIH and sickened and polished off so many people, including such names as Rock Hudson and Arthur Ashe, and is now threatening the black community in America as well as so many new recruits to AIDS meme thinking in Africa and Asia.

The consequences are so dire that it is almost inconceivable that a public disavowal of HIV will ever take place at the top level, where it should take place, if those perched there were ever to meet their public responsibility in the matter.

This is the hippopotamus in the HIV=AIDS bath, so to speak, the unacknowledged problem all sophisticated observers can see, regardless of which side they fight on in public, that is to say, whether they still promote the now thoroughly debunked paradigm, or whether they are debunkers who struggle to get coverage of its utterly specious and indefensible nature into the mainstream media.

Media, that is, served by science reporters who have absolutely no interest in going up against the solid array of authority figures, scientific institutions, governments and international organizations around the world who have signed on to the paradigm as instructed by Science, Nature and the rest of the supposedly authoritative scientific journals we all know and trust, until we find out how wrong they can be.

A solution appears, hidden in Specter’s piece

But now we have a solution of how to make this transition so no one gets hurt, thanks to the fellow traveling HIV=AIDS reporter Specter, who as usual clearly has no idea at all as to the truth or falsehood of any of the material he covers in this field, but merely acts as an excellent conduit of the claims and interpretations of the fine scientists he talks to into the pages of the indispensable New Yorker, a very fine magazine that we all know and trust.

Trust until, that is, until we find out how wrong it can be if its superb reporters don’t somehow find some way to employ a little investigation on their own when dealing with scientists, who are after all as human as the rest of us, and therefore likely to include one or two bad apples who try to pull the wool over the eyes of unsuspecting, politely uncritical interpreters of their story such as the inimitable Specter.

See if you can detect the exit door to the HIV=AIDS global debacle opened by the presumably unwitting Michael in this story, which was in the December 3 issue and is now available in full at Darwin’s Surprise: Why are evolutionary biologists bringing back extinct deadly viruses?

Or you can read it here:
From the December 3 issue of the New Yorker
at http://www.newyorker.com/reporting/2007/12/03/071203fa_fact_specter?printable=true
Darwin’s Surprise Why are evolutionary biologists bringing back extinct deadly viruses?
by Michael Specter
December 3, 2007

Disabled retroviruses-fossils of molecular battles that raged for generations-make up eight per cent of the human genome.

Thierry Heidmann’s office, adjacent to the laboratory he runs at the Institut Gustave Roussy, on the southern edge of Paris, could pass for a museum of genetic catastrophe. Files devoted to the world’s most horrifying infectious diseases fill the cabinets and line the shelves. There are thick folders for smallpox, Ebola virus, and various forms of influenza. SARS is accounted for, as are more obscure pathogens, such as feline leukemia virus, Mason-Pfizer monkey virus, and simian foamy virus, which is endemic in African apes. H.I.V., the best-known and most insidious of the viruses at work today, has its own shelf of files. The lab’s beakers, vials, and refrigerators, secured behind locked doors with double-paned windows, all teem with viruses. Heidmann, a meaty, middle-aged man with wild eyebrows and a beard heavily flecked with gray, has devoted his career to learning what viruses might tell us about AIDS and various forms of cancer. “This knowledge will help us treat terrible diseases,” he told me, nodding briefly toward his lab. “Viruses can provide answers to questions we have never even asked.”

Viruses reproduce rapidly and often with violent results, yet they are so rudimentary that many scientists don’t even consider them to be alive. A virus is nothing more than a few strands of genetic material wrapped in a package of protein—a parasite, unable to function on its own. In order to survive, it must find a cell to infect. Only then can any virus make use of its single talent, which is to take control of a host’s cellular machinery and use it to churn out thousands of copies of itself. These viruses then move from one cell to the next, transforming each new host into a factory that makes even more virus. In this way, one infected cell soon becomes billions.

Nothing—not even the Plague—has posed a more persistent threat to humanity than viral diseases: yellow fever, measles, and smallpox have been causing epidemics for thousands of years. At the end of the First World War, fifty million people died of the Spanish flu; smallpox may have killed half a billion during the twentieth century alone. Those viruses were highly infectious, yet their impact was limited by their ferocity: a virus may destroy an entire culture, but if we die it dies, too. As a result, not even smallpox possessed the evolutionary power to influence humans as a species—to alter our genetic structure. That would require an organism to insinuate itself into the critical cells we need in order to reproduce: our germ cells. Only retroviruses, which reverse the usual flow of genetic code from DNA to RNA, are capable of that. A retrovirus stores its genetic information in a single-stranded molecule of RNA, instead of the more common double-stranded DNA. When it infects a cell, the virus deploys a special enzyme, called reverse transcriptase, that enables it to copy itself and then paste its own genes into the new cell’s DNA. It then becomes part of that cell forever; when the cell divides, the virus goes with it. Scientists have long suspected that if a retrovirus happens to infect a human sperm cell or egg, which is rare, and if that embryo survives—which is rarer still—the retrovirus could take its place in the blueprint of our species, passed from mother to child, and from one generation to the next, much like a gene for eye color or asthma.

When the sequence of the human genome was fully mapped, in 2003, researchers also discovered something they had not anticipated: our bodies are littered with the shards of such retroviruses, fragments of the chemical code from which all genetic material is made. It takes less than two per cent of our genome to create all the proteins necessary for us to live. Eight per cent, however, is composed of broken and disabled retroviruses, which, millions of years ago, managed to embed themselves in the DNA of our ancestors. They are called endogenous retroviruses, because once they infect the DNA of a species they become part of that species. One by one, though, after molecular battles that raged for thousands of generations, they have been defeated by evolution. Like dinosaur bones, these viral fragments are fossils. Instead of having been buried in sand, they reside within each of us, carrying a record that goes back millions of years. Because they no longer seem to serve a purpose or cause harm, these remnants have often been referred to as “junk DNA.” Many still manage to generate proteins, but scientists have never found one that functions properly in humans or that could make us sick.

Then, last year, Thierry Heidmann brought one back to life. Combining the tools of genomics, virology, and evolutionary biology, he and his colleagues took a virus that had been extinct for hundreds of thousands of years, figured out how the broken parts were originally aligned, and then pieced them together. After resurrecting the virus, the team placed it in human cells and found that their creation did indeed insert itself into the DNA of those cells. They also mixed the virus with cells taken from hamsters and cats. It quickly infected them all, offering the first evidence that the broken parts could once again be made infectious. The experiment could provide vital clues about how viruses like H.I.V. work. Inevitably, though, it also conjures images of Frankenstein’s monster and Jurassic Park.

“If you think about this for five minutes, it is wild stuff,” John Coffin told me when I visited him in his laboratory at Tufts University, where he is the American Cancer Society Research Professor. Coffin is one of the country’s most distinguished molecular biologists, and was one of the first to explore the role of endogenous retroviruses in human evolution. “I understand that the idea of bringing something dead back to life is fundamentally frightening,” he went on. “It’s a power that science has come to possess and it makes us queasy, and it should. But there are many viruses that are more dangerous than these—more infectious, far riskier to work with, and less potentially useful.’’

Thanks to steady advances in computing power and DNA technology, a talented undergraduate with a decent laptop and access to any university biology lab can assemble a virus with ease. Five years ago, as if to prove that point, researchers from the State University of New York at Stony Brook “built” a polio virus, using widely available information and DNA they bought through the mail. To test their “polio recipe,” they injected the virus into mice. The animals first became paralyzed and then died. (“The reason we did it was to prove that it can be done,’’ Eckard Wimmer, who led the team, said at the time. “Progress in biomedical research has its benefits and it has its downside.’’) The effort was widely seen as pointless and the justification absurd. “Proof of principle for bioterrorism,’’ Coffin called it. “Nothing more.” Then, two years ago, after researchers had sequenced the genetic code of the 1918 flu virus, federal scientists reconstructed it, too. In that case, there was a well-understood and highly desired goal: to develop a vaccine that might offer protection against future pandemics.

Resurrecting an extinct virus is another matter. Still, if Heidmann had stuck to scientific nomenclature when he published his results, last fall, few outside his profession would have noticed. A paper entitled “Identification of an Infectious Progenitor for the Multiple-Copy HERV-K Human Endogenous Retroelements,’’ which appeared in the journal Genome Research, was unlikely to cause a stir. Heidmann is on a bit of a mission, though. He named the virus Phoenix, after the mythical bird that rises from the ashes, because he is convinced that this virus and others like it have much to tell about the origins and the evolution of humanity.

With equal ardor but less fanfare, scientists throughout the world have embarked on similar or related projects. One team, at the Aaron Diamond AIDS Research Center, in New York, recently created an almost identical virus. In the past few months, groups at Oxford University and at the Fred Hutchinson Cancer Research Center, in Seattle, have also produced results that provide startling observations about evolution and disease. The approaches often differ, but not the goals. All of these researchers hope that excavating the molecular past will help address the medical complexities that we confront today. Almost incidentally, they have created a new discipline, paleovirology, which seeks to better understand the impact of modern diseases by studying the genetic history of ancient viruses.

“This is something not to fear but to celebrate,’’ Heidmann told me one day as we sat in his office at the institute, which is dedicated to the treatment and eradication of cancer. Through the window, the Eiffel Tower hovered silently over the distant city. “What is remarkable here, and unique, is the fact that endogenous retroviruses are two things at once: genes and viruses. And those viruses helped make us who we are today just as surely as other genes did. I am not certain that we would have survived as a species without them.”

He continued, “The Phoenix virus sheds light on how H.I.V. operates, but, more than that, on how we operate, and how we evolved. Many people study other aspects of human evolution—how we came to walk, or the meaning of domesticated animals. But I would argue that equally important is the role of pathogens in shaping the way we are today. Look, for instance, at the process of pregnancy and birth.’’ Heidmann and others have suggested that without endogenous retroviruses mammals might never have developed a placenta, which protects the fetus and gives it time to mature. That led to live birth, one of the hallmarks of our evolutionary success over birds, reptiles, and fish. Eggs cannot eliminate waste or draw the maternal nutrients required to develop the large brains that have made mammals so versatile. “These viruses made those changes possible,’’ Heidmann told me. “It is quite possible that, without them, human beings would still be laying eggs.”

H·I.V., the only retrovirus that most people have heard of, has caused more than twenty-five million deaths and infected at least twice that number of people since the middle of the twentieth century, when it moved from monkey to man. It may be hard to understand how organisms from that same family, and constructed with the same genes, could have played a beneficial, and possibly even essential, role in the health and development of any species. In 1968, Robin Weiss, who is now a professor of viral oncology at University College London, found endogenous retroviruses in the embryos of healthy chickens. When he suggested that they were not only benign but might actually perform a critical function in placental development, molecular biologists laughed. “When I first submitted my results on a novel ‘endogenous’ envelope, suggesting the existence of an integrated retrovirus in normal embryo cells, the manuscript was roundly rejected,’’ Weiss wrote last year in the journal Retrovirology. “One reviewer pronounced that my interpretation was impossible.’’ Weiss, who is responsible for much of the basic knowledge about how the AIDS virus interacts with the human immune system, was not deterred. He was eager to learn whether the chicken retroviruses he had seen were recently acquired infections or inheritances that had been passed down through the centuries. He moved to the Pahang jungle of Malaysia and began living with a group of Orang Asli tribesmen. Red jungle fowl, an ancestor species of chickens, were plentiful there, and the tribe was skilled at trapping them. After collecting and testing both eggs and blood samples, Weiss was able to identify versions of the same viruses. Similar tests were soon carried out on other animals. The discovery helped mark the beginning of a new approach to biology. “If Charles Darwin reappeared today, he might be surprised to learn that humans are descended from viruses as well as from apes,” Weiss wrote.

Darwin’s surprise almost certainly would be mixed with delight: when he suggested, in “The Descent of Man” (1871), that humans and apes shared a common ancestor, it was a revolutionary idea, and it remains one today. Yet nothing provides more convincing evidence for the “theory” of evolution than the viruses contained within our DNA. Until recently, the earliest available information about the history and the course of human diseases, like smallpox and typhus, came from mummies no more than four thousand years old. Evolution cannot be measured in a time span that short. Endogenous retroviruses provide a trail of molecular bread crumbs leading millions of years into the past.

Darwin’s theory makes sense, though, only if humans share most of those viral fragments with relatives like chimpanzees and monkeys. And we do, in thousands of places throughout our genome. If that were a coincidence, humans and chimpanzees would have had to endure an incalculable number of identical viral infections in the course of millions of years, and then, somehow, those infections would have had to end up in exactly the same place within each genome. The rungs of the ladder of human DNA consist of three billion pairs of nucleotides spread across forty-six chromosomes. The sequences of those nucleotides determine how each person differs from another, and from all other living things. The only way that humans, in thousands of seemingly random locations, could possess the exact retroviral DNA found in another species is by inheriting it from a common ancestor.

Molecular biology has made precise knowledge about the nature of that inheritance possible. With extensive databases of genetic sequences, reconstructing ancestral genomes has become common, and retroviruses have been found in the genome of every vertebrate species that has been studied. Anthropologists and biologists have used them to investigate not only the lineage of primates but the relationships among animals—dogs, jackals, wolves, and foxes, for example—and also to test whether similar organisms may in fact be unrelated.

Although it is no longer a daunting technical task to find such viruses, or their genes, figuring out the selective evolutionary pressures that shaped them remains difficult. Partly, that is because the viruses mutate with such speed. H.I.V. can evolve a million times as fast as the human-immune-system cells it infects. (Such constant change makes it hard to develop antiviral drugs that will remain effective for long, and it has also presented a significant obstacle to the development of an AIDS vaccine.)

There are retroviruses (like H.I.V.) that do not infect sperm or egg cells. Because they are not inherited, they leave no trace of their history. “We can have a fossil record only of the viruses that made it into the germ line,’’ Paul Bieniasz told me. “And, of course, most did not.” Bieniasz is a professor of retrovirology at the Aaron Diamond AIDS Research Center and the chief of the retrovirology laboratory at Rockefeller University. He has long been interested in the way complex organisms interact with viruses and adapt to them. “With flu virus, you can watch it change in real time,’’ he said. “You can watch the antibodies develop and see when and how it dies out. But with these others you are looking back tens of millions of years, so it is hard to know how a virus functioned.’’

While Heidmann was working with the Phoenix virus in France, Bieniasz and two colleagues at Aaron Diamond initiated a similar project. (At first, neither team was aware of the other’s work.) Bieniasz rebuilt the youngest extinct retrovirus in the human genome—one that was still active a few hundred thousand years ago—because it had the fewest mutations. The team took ten versions of that virus (we carry more than thirty) and compared the thousands of nucleotides in the genetic sequence of each version. They were almost identical, but where they differed the researchers selected the nucleotides that appeared most frequently. That permitted them to piece together a working replica of the extinct retrovirus. “If you have a person with a lethal defect in the heart,’’ Bieniasz explained, “and another with a lethal defect in the kidney, you could make one healthy person by transplanting the respective organs. That is what we did.

“In the past, you got sick and you keeled over and died,’’ he said. “Or you survived. Nobody could make much sense of it. But almost ten per cent of our DNA consists of old retroviruses, and that says to me that it’s pretty clear they played a major role in our evolution. We evolved remarkably sophisticated defenses against them, and we would have done that only if their impact on human populations had been quite severe. It’s very likely that we have been under threat from retroviruses many times throughout human history. It is eminently possible that this is not the first time we have been colonized by a virus very much like H.I.V.”

At the end of the nineteenth century, a mysterious series of cancer epidemics devastated American poultry farms. One bird would fall ill and the entire flock would soon be dead. In 1909, a desperate farmer from Long Island brought a chicken with a tumor to the laboratory of Peyton Rous, a young cancer researcher at the Rockefeller Institute for Medical Research, in New York City (which became Rockefeller University). Cancer was not supposed to spread by virus, but the bird clearly had cancer. Rous, who as a young man worked on a Texas cattle ranch, was mystified. He extracted cancer cells from the sick bird, chopped them up, and injected the filtered remains into healthy chickens: they all developed tumors. A virus had to be the cause, but for years no one could figure out how the virus functioned.

Then, in the nineteen-sixties, Howard Temin, a virologist at the University of Wisconsin, began to question the “central dogma” of molecular biology, which stated that genetic instructions moved in a single direction, from the basic blueprints contained within our DNA to RNA, which translates those blueprints and uses them to build proteins. He suggested that the process could essentially run in the other direction: an RNA tumor virus could give rise to a DNA copy, which would then insert itself into the genetic material of a cell. Temin’s theory was dismissed, like most fundamental departures from conventional wisdom. But he never wavered. Finally, in 1970, he and David Baltimore, who was working in a separate lab, at the Massachusetts Institute of Technology, simultaneously discovered reverse transcriptase, the special enzyme that can do exactly what Temin predicted: make DNA from RNA.

The discovery has had a profound impact on modern medicine. It not only explained how cancer can be caused by a virus but provided researchers with the tools they needed to understand the origins and natural progression of diseases like AIDS. It also created a new field, retrovirology, and, more than that, as the Nobel committee noted when it awarded the 1975 Prize in Medicine to both Baltimore and Temin, it began to erase the tenuous borders between viruses and genes.

Retroviruses cause cancers in chickens, sheep, mice, and other animals, but their effect on humans became clear only in the late nineteen-seventies, with the identification of two viruses that cause forms of leukemia. Retroviral proteins are particularly abundant in certain kinds of tumor cells, and scientists wondered to what degree they might be a cause of cancer. They were also curious about how retroviruses that infect us today differ from their ancestors. Working with mice in 2005, Thierry Heidmann found that endogenous retroviruses were present in large quantities in tumor cells. Similar viruses have been associated with many cancers (and other diseases). It is still not clear how they function, but they may help subvert the immune system, which would permit cancer cells to grow without restraint. Endogenous retroviruses also may actually protect us from viruses that are even worse. Experiments with mice and chickens have shown that they can block new infections by viruses with a similar genetic structure. Nonetheless, endogenous retroviruses are parasites, and in most cases the cells they infect would be better off without them. There is, however, one notable exception.

The earliest mammals, ancestors of the spiny anteater and the duck-billed platypus, laid eggs. Then, at least a hundred million years ago, embryos, instead of growing in a shell, essentially became parasites. While only balls of cells, they began to implant themselves in the lining of the womb. The result was the placenta, which permits the embyros to take nourishment from the mother’s blood, while preventing immune cells or bacteria from entering. The placenta is essentially a modified egg. In the early nineteen-seventies, biologists who were scanning baboon placentas with an electron microscope were surprised to see retroviruses on a layer of tissue known as the syncytium, which forms the principal barrier between mother and fetus. They were even more surprised to see that all the animals were healthy. The same phenomenon was soon observed in mice, cats, guinea pigs, and humans. For many years, however, embryologists were not quite sure what to make of these placental discoveries. Most remained focussed on the potential harm a retrovirus could cause, rather than on any possible benefit. Cell fusion is a fundamental characteristic of the mammalian placenta but also, it turns out, of endogenous retroviruses. In fact, the protein syncytin, which causes placental cells to fuse together, employs the exact mechanism that enables retroviruses to latch on to the cells they infect.

The Nobel Prize-winning biologist Joshua Lederberg once wrote that the “single biggest threat to man’s continued dominance on this planet is the virus.” Harmit Malik, an evolutionary geneticist at the Fred Hutchinson Cancer Research Center, acknowledges the threat, yet he is confident that viruses may also provide one of our greatest scientific opportunities. Exploring that fundamental paradox—that our most talented parasites may also make us stronger—has become Malik’s passion. “We have been in an evolutionary arms race with viruses for at least one hundred million years,’’ he told me recently, when I visited his laboratory. “There is genetic conflict everywhere. You see it in processes that you would never suspect; in cell division, for instance, and in the production of proteins involved in the very essence of maintaining life.

“One party is winning and the other losing all the time,” Malik went on. “That’s evolution. It’s the world’s definitive game of cat and mouse. Viruses evolve, the host adapts, proteins change, viruses evade them. It never ends.” The AIDS virus, for example, has one gene, called “vif,” that does nothing but block a protein whose sole job is to stop the virus from making copies of itself. It simply takes that protein into the cellular equivalent of a trash can; if not for that gene, H.I.V. might have been a trivial disease. “To even think about the many million-year processes that caused that sort of evolution,” Malik said, shaking his head in wonder. “It’s dazzling.” Malik grew up in Bombay and studied chemical engineering at the Indian Institute of Technology there, one of the most prestigious technical institutions in a country obsessed with producing engineers. He gave no real thought to biology, but he was wholly uninspired by his other studies. “It was fair to say I had little interest in chemical engineering, and I happened to tell that to my faculty adviser,’’ he recalled. “He asked me what I liked. Well, I was reading Richard Dawkins at the time, his book ‘The Selfish Gene’ ”—which asserts that a gene will operate in its own interest even if that means destroying an organism that it inhabits or helped create. The concept fascinated Malik. “I was thinking of becoming a philosopher,’’ he said. “I thought I would study selfishness.”

Malik’s adviser had another idea. The university had just established a department of molecular biology, and Malik was dispatched to speak with its director. “This guy ended up teaching me by himself, sitting across the table. We met three times a week. I soon realized that he was testing out his course on me. I liked it and decided to apply to graduate school—although I had less than a tenth of the required biology courses. I had very little hope.’’ But he had excellent test scores and in 1993 was accepted at the University of Rochester, as a graduate student in the biology department. He visited his new adviser as soon as he arrived. “He looked at my schedule and said, ‘I see that you are doing genetics.’ I had no clue what he was talking about, but I said sure, that sounds good. I had never taken a course in the subject. He gave me the textbook and told me that the class was for undergraduates, which made me feel more comfortable.’’ It wasn’t until the end of the conversation that Malik realized he would be teaching the class, not taking it.

The Hutchinson Center encourages its research scientists to collaborate with colleagues in seemingly unrelated fields. Malik and Michael Emerman, a virologist at the center’s Human Biology and Basic Sciences Divisions, have been working together for four years. Malik’s principal interest is historical: why did evolutionary pressures shape our defenses against viruses, and how have they done it? Emerman studies the genetic composition and molecular pathology of the AIDS virus. “Together, we are trying to understand what constellation of viruses we are susceptible to and why,’’ Emerman told me. “We know at least that it is all a consequence of infections our ancestors had. So from there we want to try and derive a modern repertoire of antiviral genes.”

They focussed on chimpanzees, our closest relatives. Chimpanzees are easily infected by the AIDS virus, but it never makes them sick. That has remained one of the most frustrating mysteries of the epidemic. How did nearly identical genetic relatives become immune to a virus that attacks us with such vigor? The most dramatic difference between the chimp genome and ours is that chimps have roughly a hundred and thirty copies of a virus called Pan troglodytes endogenous retrovirus, which scientists refer to by the acronym PtERV (pronounced “pea-terv”). Gorillas have eighty copies. Humans have none.

“We can see that PtERV infected gorillas and chimps four million years ago,’’ Emerman told me. “But there was never any trace of its infecting humans.” It is possible that all infected humans died, but it is far more likely that we developed a way to repel the virus. Nobody knew why until Emerman, Malik, and Shari Kaiser, a graduate student in Emerman’s lab, presented evidence for a startling theory: the evolutionary process that protects us from PtERV may be the central reason we are vulnerable to H.I.V.

“We thought we must have a defense against this thing that they don’t have,’’ Malik told me, picking up the story the following day. Evolutionary biologists are not given to emotional outbursts—by definition, they take the long view. Malik is an engaging and voluble exception. When an antiviral protein excites him, he doesn’t hold back. “Where but in evolutionary history can you see a story like this, with PtERV and the chimps?’’ he asked, leaping up from his chair to begin sketching viral particles on a whiteboard. “It’s simply amazing.’’

He launched into a description of the complex interactions between viruses and the proteins that we have developed to fight them. There is one particular gene, called TRIM5a, that in humans manufactures a protein that binds to and destroys PtERV. “Our version of this gene is highly effective against PtERV, which is why we don’t get infected,’’ he said. Every primate has some version, but it works differently in each species—customized to fit the varying evolutionary requirements of each. In the rhesus monkey, that single gene provides complete protection against H.I.V. infection. In humans, it does nothing of the kind. “When Michael and I started to get into this business, people had never thought much about the evolutionary meaning of that gene. But we wondered, Is TRIM5a just an anti-H.I.V. factor or is there something else going on here?”

Like the two human retroviruses that were reconstructed in France and in New York, PtERV has long been extinct; Emerman and Malik realized that they would have to assemble a new version if they hoped to learn how we became immune to it. They took scores of viral sequences and lined them up to see what they had in common. The answer was almost everything. When there were differences in the sequence, the researchers used a statistical model to predict the most likely original version. Then they put the virus back together. (Like Bieniasz, in New York, they did so in such a way that the virus could reproduce only once.) They modified the human TRIM5a protein so that it would function like the chimp version. After that, the protein no longer protected humans against the reconstructed copy of the virus. Next, they tested this modified version against H.I.V. Emerman placed it in a dish, first with H.I.V. and next with PtERV. What he found astonished him. No matter how many times he repeated the test, the results never varied. “In every case, the protein blocked either PtERV or H.I.V.,” Emerman told me. “But it never protected the cells from both viruses.”

There are several possible ways to interpret the data, but the one favored by the researchers is that because humans developed an effective defense against one virus, PtERV, at about the time we split off from the chimps, five million years ago, we were left vulnerable to a new one, H.I.V. “If we can develop a drug that acts the same way the monkey version of this protein acts—so that it recognizes H.I.V. and neutralizes it—we could have a very effective therapy,’’ Malik said. Both he and Emerman stressed that this day will not come soon. “First, we have to establish what part of TRIM5a is actually responsible for protecting monkeys against H.I.V.,” Malik said. “Then we would have to try and make it as a drug”—and one that the human body won’t reject. “The challenge is to find out how little you can change the human version and still make it effective against H.I.V. That is really what drives this whole story of re-creating that extinct virus and doing these experiments. Nobody is doing this as a gimmick. This virus could open doors that have been closed to us for millions of years. And if we can learn how to do that we have a chance to find a very effective response to one of the world’s most incredibly effective viruses.”

The Oxford University zoology department is housed in a forbidding concrete structure that looks like an Eastern European police station. The building is named for the Dutch ethologist Niko Tinbergen, whose work—with wasps and gulls, among other species—won him a Nobel Prize and helped establish the study of animal behavior as a science. Tinbergen’s most famous student, Richard Dawkins, has carried on the university tradition of aggressive independence, and so have the younger members of the faculty. I stopped by the department a few months ago to have lunch with two of them, Aris Katzourakis and Robert Belshaw, both evolutionary biologists who have made the new field of paleovirology a specialty. Just before I arrived, Katzourakis had lobbed a bomb into the field.

Nobody knows what chain of evolutionary factors is required to transform an infectious virus—like H.I.V.—into one that is inherited. Such a virus would have to invade reproductive cells. H.I.V. doesn’t do that. It belongs to a class called lentiviruses (from the Latin for “slow”), which are common in mammals like sheep and goats. Because lentiviruses had never been found in any animal’s genome, most virologists assumed that they evolved recently. Until this summer, the oldest known lentivirus was “only” a million years, and almost no one thought that a lentivirus could become endogenous.

In a paper titled “Discovery and Analysis of the First Endogenous Lentivirus,’’ published last spring in Proceedings of the National Academy of Sciences, Katzourakis, along with collaborators from Oxford, Stanford University, and Imperial College London, showed otherwise. They discovered the fossilized remains of an ancient lentivirus—the same type that causes AIDS—within the genome of the European rabbit (Oryctolagus cuniculus). “At first, I just assumed it was a mistake,’’ Katzourakis told me over lunch in the building’s cafeteria, Darwin’s Café. “We checked it twice, three times. But we kept seeing genes that are found only in lentiviruses.’’ They named their discovery “rabbit endogenous lentivirus type K,” or RELIK. An obvious next step for Katzourakis and his group will be to work with virologists who can assemble a functional version of the ancient virus—as the researchers in Paris, New York, and Seattle have done. “It’s the most promising way to explore the evolution and the impact of H.I.V.,” he said.

It might be more than that. AIDS researchers have always been handicapped by the absence of a small-animal model in which to study the effects of the disease. It is not easy to use monkeys or sheep. They are expensive and difficult to obtain, and, for reasons of ethics, many experiments on them are proscribed. “Although RELIK is an ancient lentivirus and only defective copies were identified in this analysis,’’ the authors wrote, “recent research has shown that it is possible to reconstruct infectious progenitors of such viruses,” which, they concluded, could potentially “provide a small animal model for experimental research.”

The discovery has already changed the way scientists think about viral evolution, and about H.I.V. in particular. “The most obvious implication is that we can no longer say that H.I.V. could not become endogenous,’’ John Coffin, of Tufts, told me, though he still considers that unlikely. “It opens the field to a whole new level of examination.” It also considerably alters the phylogenetic tree. RELIK is at least seven million years old, which makes it the oldest known lentivirus. “It is possible that primate lentiviruses such as H.I.V. and S.I.V.’’—its simian cousin—“are much older than people ever thought,” Coffin said.

We can’t be certain when endogenous retroviruses entered our genome, because it is impossible to watch a five-million-year process unfold. Yet in Australia a retrovirus seems to be evolving in front of our eyes. Beginning in the late nineteenth century, koalas on the mainland were hunted nearly to extinction. To protect them, as many as possible were captured and moved to several islands in the south. In the past hundred years, those koalas have been used to replenish the population on the mainland and on several other Australian islands. In many cases, though, they have become infected with a retrovirus that causes leukemia, immune disorders, and other diseases. It can even kill them. The epidemic presents a significant threat to the future of the species, and scientists have followed it closely. One group, from the University of Queensland, looked for the virus in koala DNA—and, as one would expect with a retrovirus, found it. The team also noticed that some of the babies, known as joeys, were infected in the same locations on their DNA as their parents. That means that the virus has become endogenous. Yet, when the scientists examined the koalas on Kangaroo Island, in the south, they discovered something they had not anticipated: none of the koalas were infected.

That could mean only one thing: since the infected animals had all been moved just in the past century, the koala retrovirus must have spread to Australia recently and is entering the genome now. That offers virologists and evolutionary biologists their first opportunity to learn how a virus transforms itself from something that can simply infect (and kill) its host to an organism that will become a permanent part of that host. Persistent viruses tend to grow weaker over the years. They couldn’t live for long if they killed everything they infected. How they adapt, though, is a mystery. “Events like this have obviously occurred in human evolution,’’ Paul Bieniasz told me—even with viruses like H.I.V. “We might be able to see how the koala infection settles into the genome, and whether it plays a role in helping its host fend off other viruses,” he continued. “Whatever we learn will be useful, because we could never have learned it in any other way.”

In 1963, Linus Pauling, the twentieth century’s most influential chemist, wrote an essay, with Emile Zuckerkandl, in which they predicted that it would one day become possible to reconstruct extinct forms of life. It has taken half a century for scientists to acquire the information necessary to master most of the essential molecular biology and genetics, but there can no longer be any doubt that Pauling was right. Once you are able to assemble the ancestral sequence of any form of life, all you have to do is put the genes together, and back it comes.

“The knowledge you gain from resurrecting something that has not been alive for a million years has to be immensely valuable,’’ Harmit Malik told me in Seattle. “We didn’t take it lightly, and I don’t think any of our colleagues did, either.’’ He repeatedly pointed out that each virus was assembled in such a way that it could reproduce only once. “If you can’t apply the knowledge, you shouldn’t do the experiment,” he said. Malik is a basic research scientist. His work is not directly related to drug development or treating disease. Still, he thinks deeply about the link between what he does and the benefits such work might produce. That is an entirely new way to look at the purpose of scientific research, which in the past was always propelled by intellectual curiosity, not utilitarian goals. Among élite scientists, it was usually considered gauche to be obsessed with anything so tangible or immediate; brilliant discoveries were supposed to percolate. But that paradigm was constructed before laboratories around the world got into the business of reshaping, resurrecting, and creating various forms of life.

The insights provided by recent advances in evolutionary biology have already been put to use, particularly in efforts to stop the AIDS virus. One of the main reasons that endogenous retroviruses can enter our genome without killing us is that they make many errors when they reproduce. Those errors are genetic mutations. The faster a cell reproduces (and the older it is), the more errors it is likely to make. And the more errors it makes the less likely it is to be dangerous to its host. “Viruses are accumulating and becoming more decrepit with every passing million years” was the way Malik described it to me. That realization has led AIDS researchers to contemplate a novel kind of drug. Until recently, antiviral medications had been designed largely to prevent H.I.V. from reproducing. Various drugs try to interfere with enzymes and other proteins that are essential for the virus to copy itself. There is a problem with this approach, however. Because the virus changes so rapidly, after a while a drug designed to stop it can lose its effectiveness completely. (That is why people take cocktails of H.I.V. medications; the combinations help slow the rate at which the virus learns to evade those interventions.)

Scientists at a company called Koronis Pharmaceuticals, just outside Seattle, are taking the opposite approach. They hope that by speeding up the life cycle of the AIDS virus they can drive it to extinction. The goal is to accelerate the virus’s already rapid pace of mutation to the point where it produces such an enormous number of errors in its genome that it ceases to pose a threat. Like endogenous retroviruses, H.I.V. would become extinct. Earlier this month, researchers at the University of California at San Francisco and at the University of Toronto announced an even more fascinating way to use the fossils in our genome. H.I.V. infects immune-system cells and alters them so that they can produce more H.I.V. In doing so, they stimulate endogenous retroviruses, which then produce proteins that act as a sort of distress signal. Those signals can be detected on the surface of H.I.V.-infected cells, and in theory it should be possible to develop vaccines that target them. In essence, such a vaccine would act like a smart bomb, homing in on a signal transmitted from within each H.I.V.-infected cell. The team in San Francisco found strong evidence of those signals in the immune cells of fifteen of sixteen volunteers who were infected with H.I.V. In an uninfected control group, the signals were far weaker or were absent altogether. “For a vaccine against an infectious agent, this is a completely new strategy,’’ Douglas Nixon, the immunologist who led the team, said. It’s one that could not have emerged without the recent knowledge gained through experiments with endogenous retroviruses.

There may be no biological process more complicated than the relationships that viruses have with their hosts. Could it be that their persistence made it possible for humans to thrive? Luis P. Villarreal has posed that question many times, most notably in a 2004 essay, “Can Viruses Make Us Human?” Villarreal is the director of the Center for Virus Research at the University of California at Irvine. “This question will seem preposterous to most,’’ his essay begins. “Viruses are molecular genetic parasites and are mostly recognized for their ability to induce disease.” Yet he goes on to argue that they also represent “a major creative force’’ in our evolution, driving each infected cell to acquire new and increasingly complex molecular identities. Villarreal was among the first to propose that endogenous retroviruses played a crucial role in the development of the mammalian placenta. He goes further than that, though: “Clearly, we have been observing evolution only for a very short time. Yet we can witness what current viruses,” such as H.I.V., “can and might do to the human population.”

Villarreal predicts that, without an effective AIDS vaccine, nearly the entire population of Africa will eventually perish. “We can also expect at least a few humans to survive,’’ he wrote. They would be people who have been infected with H.I.V. yet, for some reason, do not get sick. “These survivors would thus be left to repopulate the continent. However, the resulting human population would be distinct” from those whom H.I.V. makes sick. These people would have acquired some combination of genes that confers resistance to H.I.V. There are already examples of specific mutations that seem to protect people against the virus. (For H.I.V. to infect immune cells, for example, it must normally dock with a receptor that sits on the surface of those cells. There are people, though, whose genes instruct them to build defective receptors. Those with two copies of that defect, one from each parent, are resistant to H.I.V. infection no matter how often they are exposed to the virus.) The process might take tens, or even hundreds, of thousands of years, but Darwinian selection would ultimately favor such mutations, and provide the opportunity for the evolution of a fitter human population. “If this were to be the outcome,’’ Villarreal wrote, “we would see a new species of human, marked by its newly acquired endogenous viruses.” The difference between us and this new species would be much like the difference that we know exists between humans and chimpanzees.

For Villarreal, and a growing number of like-minded scientists, the conclusion is clear. “Viruses may well be the unseen creator that most likely did contribute to making us human.” ♦

Hint:

““The most obvious implication is that we can no longer say that H.I.V. could not become endogenous,’’ John Coffin, of Tufts, told me, though he still considers that unlikely. “It opens the field to a whole new level of examination.” It also considerably alters the phylogenetic tree. RELIK is at least seven million years old, which makes it the oldest known lentivirus. “It is possible that primate lentiviruses such as H.I.V. and S.I.V.’’—its simian cousin—“are much older than people ever thought,” Coffin said.”

38 Responses to “Misguided Guide May Solve AIDS’s Biggest Problem”

  1. Rezaf Says:

    “Partly, that is because the viruses mutate with such speed. H.I.V. can evolve a million times as fast as the human-immune-system cells it infects. (Such constant change makes it hard to develop antiviral drugs that will remain effective for long, and it has also presented a significant obstacle to the development of an AIDS vaccine.)”

    A million times? This man didn’t read Karpas or Richman, did he?

    ” “The most obvious implication is that we can no longer say that H.I.V. could not become endogenous,’’ John Coffin, of Tufts, told me, though he still considers that unlikely. “It opens the field to a whole new level of examination.” It also considerably alters the phylogenetic tree. RELIK is at least seven million years old, which makes it the oldest known lentivirus. “It is possible that primate lentiviruses such as H.I.V. and S.I.V.’’—its simian cousin—“are much older than people ever thought,” Coffin said.

    So HIV is possibly endogenous and is much older than most thought? Say 20 years plus a few thousand… So much for being sexually transmissible. If so, that means something else is trashing the immune system and triggering this virus replication.

    “Scientists at a company called Koronis Pharmaceuticals, just outside Seattle, are taking the opposite approach. They hope that by speeding up the life cycle of the AIDS virus they can drive it to extinction. The goal is to accelerate the virus’s already rapid pace of mutation to the point where it produces such an enormous number of errors in its genome that it ceases to pose a threat. Like endogenous retroviruses, H.I.V. would become extinct.”

    I sense some contradiction here. First we are told that the rapid mutation rate is the reason why the immune system can’t keep up, and then we are told that acelerating that same mutation rate is good after all.(?) If the same line of thought is applied to a HIV infection, the immune system does precisely just that: beats the crap out of the virus, the virus mutates, becomes weaker and is crushed with even more violence. Its is a version of Hell for the virus, being beaten to a pulp for all eternity. The virus runs rampant if something else is holding back immune response.

    TS, correct me if I’m wrong, but one way to accelerate this wimpy virus mutation rate is to, for example, strengthen the immune response. Is this the way out they seek? To design a drug that does not interfere with cellular function (such as normal ARVs) and bolsters the immune response, that almost sounds like proper nutrition for everyone. Immunetherapy?
    So the transition will be from the replication inhibitor drugs to immune-power-up drugs and then to the brilliant conlusion that nutrition can power-up the immune system after all? And then everyone is happy and no one in the high-ups gets hurt.

    “Villarreal predicts that, without an effective AIDS vaccine, nearly the entire population of Africa will eventually perish. “We can also expect at least a few humans to survive,’’ he wrote. They would be people who have been infected with H.I.V. yet, for some reason, do not get sick. “These survivors would thus be left to repopulate the continent. However, the resulting human population would be distinct” from those whom H.I.V. makes sick. These people would have acquired some combination of genes that confers resistance to H.I.V. There are already examples of specific mutations that seem to protect people against the virus. (For H.I.V. to infect immune cells, for example, it must normally dock with a receptor that sits on the surface of those cells.”

    Nearly the entire population of Africa will perish…eventually. Where is the decrease in population related to “AIDS”? Poverty and starvation seem to play a bigger role in that (imaginary) decrease in Africa, that apparently “AIDS” scientists seem to eagerly desire so they can be prove their hypothesis right.
    So LTNPs are genetic saviours of humanity? So Africans are marked for extinction? So it means that all those who have African genes in their genetic heritage (Africans and South-Europeans, for example) are doomed? That explains the existence of two different pandemics, the “Western AIDS” and the “Afro-asian AIDS”? Knowing that those who stay away from toxic ARVs and live on are labelled LTNPs, this seems so ridiculous.

  2. MartinDKessler Says:

    Every time dissident bloggers invoke HIV or treatment of HIV or HIV infection, the “brand” HIV is being advertised. It plays into the establishment’s view even though what dissident bloggers ( and other dissidents) say about HIV is rejected by the establishment. How do we know that anyone is “infected” with HIV? Is it because we believe what the doctors, scientists , epidemiologists, and goverment health agencies (CDC & NIH) tell us? The tests currently used are invalid much less unreliable, the grand majority of “AIDS” cases in Africa are presumed HIV infection. In my opinion, no one has been infected by this mysterious non-existent retrovirus. That would explain why the “AIDS” has not spread like conventional infectious diseases left untreated would spread (Farr’s Law). Maybe my line of thinking is radical – ie going to the root of what’s going on here, but I think as long as we keep going back to HIV, we are also blinded and hypnotized by the “brand” the establishment wants to promote.

  3. MacDonald Says:

    Hah Rezaf, if you think it’s a bit far fetched that the immune system needs help mutating HIV out of existence, you’ll have real fun with this one. According to the newest data, the best thing is if the immune system doesn’t work at all. . .

    HIV-1 infection leads to intense and sustained activation of many key components of the immune system from the very earliest stages of infection7, and this is thought to be fundamental to the system’s ultimate collapse8. An emerging scenario portrays a chronic state of heightened immune activation, which drives viral replication alongside proliferation and subsequent activation induced cell death, or apoptosis, of memory T cells (both CD4+ and CD8+). Although powerful homeostatic mechanisms endeavor to restore the T cell pool, the supply fails to keep pace with the demands posed by the high levels of T cell death and destruction, not least because thymic function is significantly impaired in HIV-1 infection9. In keeping with this hypothesis, levels of immune activation in HIV-1 infection (assessed by such indicators as the proportion of circulating CD38+DR+ T cells or serum concentration of β2 microglobulin) are closely correlated with disease progression and seem to be more accurate predictors of HIV disease than CD4+ cell count or viral load10. Further support comes from the observation that SIV-infected sooty mangabeys do not experience immune activation despite high levels of viral replication and that this is associated with the absence of disease11. Similarly, the majority of HIV-2– infected subjects who remain free from HIV induced immunosuppression show negligible immune activation, whereas immune activation in progressors with HIV-2 is comparable to that seen in HIV-1 infection12

    Oh, and by the way, for any African readers or others who might conceivably test positive from the HIV-2 molecular signature, stop taking the meds and start making love again, you’re officially in the clear now:

    Other retroviruses, such as HIV-2 and HTLV-1, infect circulating CD4+ T cells to a similar extent, yet these infections are compatible with a normal and healthy life in the majority of infected people

    This is all from a brand new article by Sarah Rowland-Jones & Tao Dong in Nature.com

    (To Roy from Aetiology, if you are reading (of course you are, naughty boy), I’m still waiting for my $50,000 for “predicting” correctly that the meme has already flipped, the HIV god is dead. It’s just that the HIV priests haven’t yet realized the extent of their deed.)

  4. Rezaf Says:

    MacD, so that implies that the virus is harmless, right? It is their admission that HIV stands for Harmless Innocent Virus. But if the immune system is rallying the troops, something else must be bombing the place. Most likely it is one of those other factors that most of us know. I vote for malnutrition being a decisive one. Without supplies, there are no guns and resources for our soldiers and factories.

    Martin, I agree. To brandish the words HIV and AIDS is, in certain way, playing into the Meme thought. But how should we address these entities, being hypothetical? Their effect in people’s minds is quite real.
    Harmless Innocent Virus is a way to do it, no? Hardly Imputable Virus? Absolutely Icredible Distortion of Science for “AIDS”, perhaps?

  5. MacDonald Says:

    Rezaf,

    Yes! You basically have a so called “Human Immunodeficiency Virus” which admittedly doesn’t cause immunodeficiency under normal circumstances. There’s no debating this point anymore.

    They supposedly isolated and sequenced the bugger + looked at the epidemiology and decided it was an “HIV”. They were wrong. If they can be wrong once why not twice?

    The idea is that HIV-2 possesses a gene product, lacking in HIV-1, that can downregulate an exaggerated immune response:

    Activation may also be related to specific activities of HIV gene products, such as nef: the nef protein of less pathogenic retroviruses has the ability to downregulate the T cell receptor–CD3
    complex, thereby protecting the cell from unwanted activation, while HIV-1 nef lacks this property15. Whereas a range of checks and balances in the healthy host should limit excessive immune activation, the susceptibility of regulatory T cells to HIV-1 infection may effectively remove a key control mechanism16.
    Reference 16 – Oswald-Richter, K. et al. PLoS Biol. 2, e198 (2004) http://biology.plosjournals.org/perlserv/?request=get
    document&doi=10.1371/journal.pbio.0020198

    This positing of different biological properties in viruses with the same name and supposedly same unique pathogenic effect is. . . well, anything goes then.

    The first question is the one you asked above: What happens when HIV-2 supposedly does manage to cause AIDS? The answer is again the one you’ve given: “Cofactors”

    Regardless, it’s a mess. Read if you will reference 16 and tell me if you’re convinced this downregulatory “nef gene product” spells the difference between perfect health and AIDS.

  6. MacDonald Says:

    Ref. 16:

    This one works for me

    http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pbio.0020198

  7. patrick moore Says:

    H armless I nnocent V irus…good one :)

  8. MartinDKessler Says:

    H (armless) I (nnocent) V (irus) Hmmm. What ever re-interpreted acronym/abbreviation is ascribed, show me the statistics of who has had the (retro)virus isolated from them or proven to have the bug in them using some “validated” method. Or do I have to accept (which I will not until validation is demonstrated) the current flawed procedure? At this time that’s the way everyone seems to be talking. Another question, what precentage of so-called AIDS victims or people with “Full Blown AIDS” actually have immune system problems. What percentage of ICL (ideopathic CD4+ lymphocytopenia – the name for people who have AIDS but didn’t register a positive result) victims had immune system problems. From an epidemiological standpoint shouldn’t those groups (AIDS with immune problems and AIDS without immune problems) represent different diseases? Or is AIDS defined ipso facto as an immune dysfunction? How about those with a presumed AIDS diagnosis – is this epidemiology – the data collection is so sloppy, it wouldn’t pass muster for basic survey research – as John Lauritsen has written – that was his field prior to becomming a full time writer.

  9. Truthseeker Says:

    TS, correct me if I’m wrong, but one way to accelerate this wimpy virus mutation rate is to, for example, strengthen the immune response. Is this the way out they seek? To design a drug that does not interfere with cellular function (such as normal ARVs) and bolsters the immune response, that almost sounds like proper nutrition for everyone. Immunetherapy?
    So the transition will be from the replication inhibitor drugs to immune-power-up drugs and then to the brilliant conlusion that nutrition can power-up the immune system after all? And then everyone is happy and no one in the high-ups gets hurt.

    Well, Rezaf, to tell you the truth you hit upon the paragraph I meant the first time:

    ” “The most obvious implication is that we can no longer say that H.I.V. could not become endogenous,’’ John Coffin, of Tufts, told me, though he still considers that unlikely. “It opens the field to a whole new level of examination.” It also considerably alters the phylogenetic tree. RELIK is at least seven million years old, which makes it the oldest known lentivirus. “It is possible that primate lentiviruses such as H.I.V. and S.I.V.’’—its simian cousin—“are much older than people ever thought,” Coffin said.

    HIV will become endogenous! The wonderful drugs used against it will have persuaded it to become part of the genome in a harmless manner that will fit the real data, so that no longer has to be denied and manipulated mercilessly, and everyone can go home and count their blessings and their profit, and move on, except for the drug companies, who can be left administering Kool Aid to Africans and Asians to ensure that they absorb their HIV into their genome too, just like Westerners.

    MacD should be happy about that, and poster here Nick Naylor too. Like many people they seem to think that HIV has been around forever and is endogenous already.

    Am I talking nonsense? Well you will have to forgive me since this field has been talking nonsense en masse from the start. But there is one thing certain – they have to find a way out of this mess without admitting they caused it by mistaking HIV for a Harm Intending Virus in the first place, now they have discovered it is really a Harmless Innocent Virus, as Rezaf seems to have labeled it rather nicely.

    MacD can you be clearer, this is Christmas and it is hard for those of us who see no merit in anything these guys babble to track exactly what it is you are saying unless they have AZT in their eggnog.

    Absolutely Incredible Distortion of Science for “AIDS”, perhaps?

    That’s a good one too. Rezaf, I thought English was not your mother tongue, but Portuguese or Spanish?

  10. Rezaf Says:

    Martin,
    What I’ve learned from most of you and the literature provided by dissent is that there are no validated methods for detecting that virus. Those that are employed don’t detect it. I have no statistics for you because no one can actually “see” this fiend. So, like you, I don’t accept the current procedures. I fear them, even, for whatever impact they might have on a person’s life after being diagnosed with something that is not there. And even being a complete ignorant in virology, I thought that to prove the existence of such virus and its effects, one would really have to isolate, purify and take a picture of the bug. The pictures I’ve seen resemble anything but viruses. I was surprised to know (a long ago) that no such thing was ever properly made for this virus. You have a point in saying that one is talking about something that might not even be what it is supposed to be. It might not even be. And a lot of research was made by searching in the wrong place and in the wrong direction. But how should one talk about this with those who still support the failed hypothesis without using the same labels/acronyms, etc?

    About your other questions, to my (limited) knowledge, there were no experiments carried out with proper controls to find out if this HIV=AIDS (sorry…) hypothesis is correct. Without a proven causation, there is no point in labelling people with “AIDS” just because they had positive on a flawed testing technique that doesn’t detect the alleged pathogen. Again, I have no percentages to offer you. You most probably know them better than I do. I can’t really answer you much. Though what I’ve learned also is that one with a perfect health can be labelled with “AIDS” ( being whatever that is ), based on a presumed diagnosis. It all seems like a big mess to me.

    MacD,

    I’ve read the paper. And I have to read it again, because there I have not found a reasonable mechanism for immune shutdown. First, the virus just depletes T-cells by infecting them and killing. These gus say that such only happens with regulatory T-cells. The loss of such cells will cause overproduction of the other T-cells and T-cell storage will be depleted. Overproduction, heh? Forgive my ignorance, why is it always assumed that T-cells exist only in limited supply throughout one’s lifetime (like braincells) and will be eventually depleted? Isn’t the function of the bone marrow and thymus also the very replenishment of these cells?
    They also speak of homeostatic equilibrium. So an overproduction of T-cells would send a negative feedback to the production facilities and tell these to slow down production until normal levels are restored. Since Treg cells are also replenishable, I assume there is some sort of equilibrium for this type of cell and any loss reported would send a positive feedback to the production facilities and order the production of more Treg cells. Was there any disruption in this equilibrium to be expected in the first place?
    Wouldn’t an overproduction of T-cells produce an even more vigorous immune response against whatever this excuse for a virus has to offer?
    But the text is a bit hard for me to read. I’ll have another look.

  11. Rezaf Says:

    “First, the virus just depletes T-cells by infecting them and killing. These gus say that such only happens with regulatory T-cells.”

    Ooops! What I meant was something like, “What? First the mainstream tells the virus just depletes T-cells by infecting them and killing. Now it tells that the immune system crashes into a wall while speed driving! What else will they think of?”
    Otherwise the paper is more of the same old stuff.

    TS,

    It does make sense. So the supposed virus genome the mainstream has could be in fact a tiny fraction of our own. Wow, we are given DNA chain terminators and other nasty stuff to fight endogenous cripples and other diluted manifestations of our own genome.

  12. Truthseeker Says:

    Rezaf, the great absurdity about this whole scene is how difficult it is for people to comprehend that the whole deal was a piece of nonsense from the word go. They have extreme difficulty in changing the fundamental premise, and think that endless discussion of what there might be in the HIV=AIDS idea is useful.

    But the truth is that a few words babbled and written by Gallo didn’t justify any of this belief, and the whole extrapolation from what he claimed is just as specious. Gallo’s claim was rubbish from the beginning, and did not deserve any of this application of seriously intelligent minds to the problem of teasing out what is true and what is not about his proposal that HIV=AIDS. It was and is the kind of crackpot notion that didn’t deserve the time of day from any serious critic, and won guffaws from everybody familiar with Gallo. Yet to most people that is inconceivable, for some reason. They cannot psychologically accept that vast crowds and august institutions and the newspaper of record can be flat out wrong.

    What it shows surely is that mental framing is all important for human evalutaion of any idea or object. This debate is really all an exercise in the psychology of how people evaluate ideas. The paradigm is a framed belief, that is, a belief that occurs and has meaning only within a framework. To change the belief you have to change the framework. Unfortunately for many people this replacement of a frame in a particular case becomes some kind of automatic skepticism applied to everything, especially government. But the key it seems to me is that it isn’t so much the rights and wrongs of the science of HIV=AIDS as the mental framework which supports and sustains it.

    Quite frankly I would say one doesnt have to know much of the science to know that the claim had to be ludicrous at the start, since the likelihood of a new science studying a hitherto unfamiliar subject, retroviruses, suddenly providing the answer to a new disease phenomenon, is almost zero. That is, for a new disease and a new science containing its solution to appear at almost exactly the same time in history is just too unlikely to take seriously. A totally new phenomenon never noted before in the history of human sickness and Bingo! a known rascal at the NIH independently and genuinely discovers in a couple of years in the very science he had chosen as a career the answer to what was causing it? How likely is that?

    To put it a better way, how likely is that soon after a new science of retroviruses is born, a new illness of great interest appears out of nowhere for the first time in human history and turns out to have a retrovirus as a cause? Somehow one doesn’t think Gallo’s prayers would earn divine intervention of this kind, however good he was at advancing himself with mortals.

  13. MacDonald Says:

    TS, can you be a little clearer about what I have to be clearer about?

    Rezaf, glad to see we’re in agreement again concerning that paper. That gives me the courage to sum up using the quote from the Jones-Dong paper:

    the susceptibility of regulatory T cells to HIV-1 infection may effectively remove a key control mechanism16

    The word “remove” implies, as Rezaf says, both that the number of T-cells is predetermined and finite, and that our immune system is so inept at adapting and compensating that, even when given a decade or two, it can find no way to deal with an undesirable reaction and regain its homeostatic equilibrium.

    This means they have to assume regulatory T-cells are indeed a “key control mechanism”, since there is apparently no conceivable pulling back from the immune system nose dive.

    Both these premises, I dare say now that Rezaf has confirmed my first impression, are pure speculation heaped on more speculation. The predictable answer from HIV enthusiasts will of course be that attacking this key control mechanism is just one, therefore not necessarily sine qua non, among the endless number of ways the endlessly resourceful, endlessly multi-tasking, endlessly mysterious tiny piece of unremarkable RNA accomplishes its deadly purpose. The HIV-AIDS hypothesis is, in other words, endlessly unfalsifiable.

    Regarding HIV-2. If we are to believe HIV scientists, this “virus” is actually much better adapted than the endlessly adaptable HIV-1, because it rarely kills its host. But if it is fitter, why is it not predominant? Ah, because it is less easily transmitted of course. See how neatly everything fits together? Except can there exist anything less easily transmitted than once in 1000-3000 intercourses. . .? How does HIV-2 survive out there in the wild West African jungles?

    One is reminded of HIV-2’s diametrical opposite, the Thai E-strain of HIV, 500 times more infectious via heterosexaul intercourse than other HIV-1 strains. It explained neatly the politically correct assumption that the explosive Thai epidemic was heterosexual and mediated by prostitutes. But if something is 500 times more transmittable than its brothers and sisters, why doesn’t this strain take over the world? Oopps, E-strain too fit to survive, so the HIV enthusiasts quickly changed their minds and decided the E-strain had the same transmission rate as all other strains.

    Martin Kessler and the rest, Dr. Maniotis has solved the linguistic problem for us. What is called HIV in orthodox-speak is now called a “molecular signature” in rethinker-speak. We acknowledge that a molecular signature is registered, but we suspend judgement as to what signed, where it came from and what it means.

    A likely explanation to HIV-2 is that this molecular signature is only expressed by certain African races, whereas the HIV-1 signature is more universal. Remember we still don’t have two identical HIV signatures from anywhere in the world, or even from the same person.

  14. Truthseeker Says:

    TS, can you be a little clearer about what I have to be clearer about?

    Rezaf, glad to see we’re in agreement again concerning that paper – MacD

    Xcellent wit, MacD, on this Xmas day, on which we send Xmas greetings to all.

    Mac D, it is hard to be clear about what I am not clear about but ideally it would be whatever you are being cryptic about as in the last sentence, instead of stating fully what it is you mean. If you only hint at it purely for the benefit of the person who already knows what you mean, it reaches one person, but perhaps not the hordes of silent onlookers crowding this theater to the rafters, at least not all ten or twelve of them, perhaps not even the slow witted host, who needs to know what you are talking about without going over it with his index finger twice speaking the long words out loud, which is sometimes the only way he manages to catch up with the essential inner truth implied but not stated in the MacD oeuvre, so original is its viewpoint and so unexpected is its conclusion.

    In other words, MacD, if you would, hew to the grand tradition of NAR and spell everything out so even the likes of the humble host can follow it, otherwise there is no hope of getting the message across to the HIV faithful if they come here to learn from their betters.

    Ideally it would be clear from the first sentence and the last sentence without having to read the sentences in between, but perhaps that is too much to ask, although it could be done at the start by saying what it is you are about to say, and finishing by saying what it is you have said.

    What I am saying here is, What the heck are you talking about, McD? Is it over my head?

  15. MacDonald Says:

    Dear Mr. Host,

    Sometimes these riddles unriddle themselves by simply rereading the previous post(s) from the poster(s) in question. Thus the paper which eludes you would be the one mentioned here:

    Reference 16 – Oswald-Richter, K. et al. PLoS Biol. 2, e198 (2004) http://biology.plosjournals.org/perlserv/?request=get
    document&doi=10.1371/journal.pbio.0020198

    AND HERE:

    Regardless, it’s a mess. Read if you will reference 16 and tell me if you’re convinced this downregulatory “nef gene product” spells the difference between perfect health and AIDS.

    AND HERE:

    MacDonald Says:
    December 24th, 2007 at 11:15 am
    Ref. 16:

    This one works for me

    http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pbio.0020198

    AND HERE:

    MacD,

    I’ve read the paper (Rezaf)
    AND HERE:

    Otherwise the paper is more of the same old stuff. (Rezaf)

    In short, the paper everybody is familiar with even they haven’t read it, and even if they read only first and last sentence of every post.

  16. Rezaf Says:

    Hmmm…

    “Otherwise the paper is more of the same old stuff. (me)”

    I guess I didn’t wrote that one well. Ooops. What I meant was that the paper draws its conclusions on the same speculations, assumptions, hypothesis, that the virus will always win. As most mainstream papers that I’ve read do. I did read this paper though.

  17. MacDonald Says:

    Rezaf,

    Again, none of this has anything to do with you. I know you’ve read the paper, twice even, and reached the exact same conclusions as the rest of us. It’s only that our dear host is confused as to which paper.

  18. Rezaf Says:

    LOL! I know, I was just correcting myself. When I read my posts again, sometimes too late, some sentences end up not making much sense.

  19. Truthseeker Says:

    It’s only that our dear host is confused as to which paper.

    MacD, the problem is more complex than that, which anyway would not be corrected by your referencing a paper with an incorrect url that goes nowhere.

    The dear host does not know what the heck you are talking about. Is there some law on the planet you speak from which forbids saying straightforwardly, like a real man, what your point is, that the paper proves to your satisfaction, which Rezaf agrees with,

    If so perhaps Rezaf can step in and give us a bottom line soundbite.

    Are you aware MacD that Einstein was renowned for making relativity intelligible to a chamber maid?

  20. Rezaf Says:

    TS,

    http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pbio.0020198&ct=1

    Hope this one works. It did for me. If you wish I can C&P the paper here. The paper dates back to ’04, so it is not that recent. I think what MacD showed me is another attempt made to explain how an excuse for a virus destroys the immune system. The way this paper put their “infection mechanism” hypothesis did not satisfy me. Like most mainstream publications on this matter, they just assume that the T-cell number is limited throughout one’s lifetime, more or less like nervous tissue cells.
    How can this be related to this topic?
    I think that the mainstream is running out of ideas on how to explain that immune dysfunction has to be linked to you-know-what. They cling to the “virus must win” condition and would rather come up with the idea that “HIV” is, for example, endogenous to explain just that, than to finally throw the towel, give in (and give way) to a full reappraisal by dissent. They will, eventually, but like you said, slowly and no heads will roll.
    I’m not saying that the idea of it being endogenous is nonsensical. It seems like a cue for that gradual shift in the paradigm that the world needs, no? The one-way ticket out of this mess.
    The mainstream is, and was, looking for a way out all the time.(?)

  21. Truthseeker Says:

    I’m not saying that the idea of it being endogenous is nonsensical. It seems like a cue for that gradual shift in the paradigm that the world needs, no? The one-way ticket out of this mess.
    The mainstream is, and was, looking for a way out all the time.(?)

    So you agree that HIV will be retired into the genome and counted inert and a victory for the marvelous drugs used to defeat it, with only the drug companies resisting, saying “Hey wait a minute! What about us?!”

    Maybe they will continue to apply the drugs even though HIV is inert, on some excuse or other. The main thing is to be able to acknowledge that HIV is not the cause of any immune dysfunction without bringing down the house, so it must be that the original HIV was aggressive, but now we have the new mutation it has been forced into by the drugs which isn’t, and now it just sits happily in the genome without doing much except keep out of the way of the immune system.

    Back to square one with a win-win declaration that modern science has triumphed and the patient is now to be dosed only when HIV mutates back into something which is dangerous, so maybe you need a good dose of DNA chain terminators then, ie when you fall ill from some other cause. Then if you fall ill and die it is because the new mutation is virulent, and to guard against this possibility we need plenty of vaccine whenever that can be developed, another $1 billion please.

    It is hard to see how this story will be presented without falling apart, but given what they have achieved to date in fairy tale bedtime stories, it can’t be beyond fixing. A lot of scriptwriters in Hollywood out of work right now, should be easy to put them to work.

  22. Rezaf Says:

    “So you agree that HIV will be retired into the genome and counted inert and a victory for the marvelous drugs used to defeat it, with only the drug companies resisting, saying “Hey wait a minute! What about us?!”

    To this day, I’m starting to doubt that HIV deserves the V. H and I would stand for a Hypothetic I-don’t-know. Being Harmless, the ARVs can only do what HIV can’t. I remember back at Aetiology, you said that the mainstream is very good at defending itself. So the endogenous idea would seem like way out for them to turn things around without anyone important being lynched by a angry mob. The Iraq situation is one example of a blatant mess with the big people responsible for it still messing around. They had sad excuses to go there and now they are looking for an excuse to get out of there. I think that big pharma is influentional enough to have a say in the role of things and come up with a way to maintain their profits. As usual, it is the people that pays for it.When will its power be contained, who can tell? What other excuses will they come up with? It is a shame, really. I would like to see this thing crumble like an imploding building for all to see.
    If they ever turn things around based on the endogenous idea, it is also a way of acknowledging the (H)armless in HIV, no? How do ruling paradigms come rolling down the hill? Isn’t the “heretic” cause finally embraced when the orthodoxy says “we knew it all along”? Nobody in the orthodoxy wants to lose their head because they were fervent defenders of a failed Hypothesis that promoted patient ostracization and poisoning over nothing. They will try to cover the hole with a lot of cushions to break their fall, definitely. But the exact outcome is hard to predict, no?
    General politics and especially the politics of “AIDS” somewhat elude me, so the probability of me saying nonsense is rather high.

  23. Carter Says:

    Back out? Exit strategy? With HIV so engrained, so endearing to those working in the field and ever so fought tooth and nail by the mainstream hierarchy, who among them would ever want an exit strategy? They first would have to want one and secondly actually know of the ways to do so. Really all they have to do to exit, either one by one or en mass, is to do what Rebecca did. Just stop and get the fuck out.

  24. Michael Says:

    If and when it all falls apart then what?

    I guess we could all just go back to enjoying good ole fashioned sex without fear, gay or straight or ???, if we arent’ too over the hill to simply enjoy it anymore. But. How boring would it be. What a letdown after the excitement of scaring the bejeebers out of my family and sexual liasons and friends and acquaintances by telling them “Don’t be ridiculous. I never get tested, and don’t worry, HIV and the HIV tests are a bunch of bull” as I watch their eyes pop wide open and I see the hairs on their neck and arms all stand at attention.

    Been there and done all that! I will certainly miss some of the fun and current excitement terribly!

    But what to do?

    To be or not to be dissident, THAT IS THE QUESTION.

    Whether tis nobler in the mind to suffer
    the slings and arrows of Tara, Noble, Moore, Gallo, and Fauci,
    And enjoy the dissidency just a bit longer,
    Or to take arms against a sea of troubles,
    And by opposing end them and risk paradigms falling,
    and becoming the mainstream
    with its boredom that is perilously close to death itself?
    To die: to sleep;
    Dissident No more; and by a sleep to say we end
    The heart-ache and the thousand natural shocks
    That AIDS Inc promotes and that the belief in HIV=AIDS is heir to.
    Ay, there’s the rub;
    For in that sleep of viral death what dreams or
    Human growth (or future nightmares) may come?
    What nightmares of other germs and viral phobias may follow?
    Or even worse nightmares of taking up basket weaving
    With Bob Gallo in an old folks home,
    or feeding squirrels on a Park Bench while
    Reminiscing with JP Moore about the “good old days”
    Of hit and run tactics on Aetiology?
    To be or Not to be? Tis surely the question.

    We dissidents must all ask ourselves this very question, and we needs must ask it soon. Do we delay our dissident armies and lighten up a bit and stretch the fun? or do we lash yet harder then ever before, and risk our own selves and our own positions as becoming the new “mainstream” beliefs?

    Perhaps this is just my fear of a life of nostalgic desperation for the good ole days that today will possibly but likely not become speaking, but perhaps we can convince Tara via some choice spams on her Aetiology Blog sight, to start a “Save JP Moore-The HIV=AIDS Half Man/Half Macaque-Campaign”, or maybe even sponsor JP Moore the HIV researcher turned Macaque for president, running on a campaign promise to eliminate world AIDS within the next 100 years. Or encourage Tara herself to run for president with such campaign promises, if the masses want a female in office. JP the Moorcaque can still at least be the poster boy for our new “Save the HIV Researchers and Macaques, Life, Livelihood, and Career Campaign”!

    Though an honorable gay or dissident knight would never do such a thing, I can’t help but to ponder such thoughts, for once the belief that HIV causes Aids is gone, it is gone, but, there are some things about it and about the struggle to overturn it, that I undoubtedly may surely miss!

  25. Truthseeker Says:

    Please don’t include schoolboy insults to the esteemed John P. Moore, microbicide tester at Weill-Cornell and chief defender and debunker of the HIV=AIDS paradigm, both, who clearly sees this collapse coming at some point and is well prepared for it. The editorial staff of Science Guardian appreciate your concern, however, at the prospect of losing the biggest, fattest and most absurd target in all of science, with all its wonderful scientific, political, and sociological manifestations, not least the rare opportunity to be right where almost everyone else, however high their position, is quite wrong. This is a very rare if not unique situation where anyone who troubles to study the situation for more than an hour can surpass in understanding most of the world in a very central topic where famous politicians jostle for advantage, top scientists vie for prizes and more than their fair share of funding, non profits, movie and rock stars cover themselves with glory by just being involved, etc. etc.

    Unfortunately, the advantages of being right in this area appear to be almost nil, except the private pleasure of knowing you are right and the rest of the world is wrong, a satisfaction freely available to almost any crackpot or conspiracy theorist without doing any research at all.

  26. Carter Says:

    Well, Michael I wouldn’t worry because there’s got to be another “Religulous” paradigm right around the corner, albeit great this one shall pass.

  27. hhbauer Says:

    About the remarkable paper MacD mentioned, Sarah Rowland-Jones & Tao Dong in Nature.com. Can anyone enlighten me about how, in the aborted vaccine trial, it was determined that vaccinated people got “infected” more than controls? Surely they can’t use antibody tests, because aren’t vaccines supposed to generate antibodies?

  28. Michael Says:

    Henry, you said: Surely they can’t use antibody tests, because aren’t vaccines supposed to generate antibodies?

    What do you mean by “Surely they can’t”? Well of course they CAN and DO use antibody tests. Antibody tests are the only tests in existence. And of course the vaccines, if they work, will generate the same antibodies.

  29. MacDonald Says:

    Mike, they actually do claim to be using tests looking for the virus itself no less.

    There are other types of HIV tests that look for the presence of the virus instead of the presence of antibodies. Participants are counseled to get HIV testing done only at their trial site because the site has access to specific tests that can differentiate between vaccine-induced positives and true HIV infection. http://www.hvtn.org/faq/503/HVTN503FAQ_eng.pdf

    The tests are not specified, but I guess it’s PCR somehow, or culture.

  30. CyrilSader Says:

    Hi all,

    I’m new here though I’m not new to the debate. I’ve been reading this blog for a while now and thought it’s about time to write.

    The New Yorker article reminds me of the point of view presented by Cal Crilly (I’m not sure if you’re already familiar with it):

    Why Retroviruses Appear in AIDS, Cancer and Autoimmune Diseases
    By Cal Crilly

    AIDS Retrovirus Expression Regulated by Methylation

    What it shows surely is that mental framing is all important for human evaluation of any idea or object. This debate is really all an exercise in the psychology of how people evaluate ideas. The paradigm is a framed belief, that is, a belief that occurs and has meaning only within a framework. To change the belief you have to change the framework. Unfortunately for many people this replacement of a frame in a particular case becomes some kind of automatic skepticism applied to everything, especially government. But the key it seems to me is that it isn’t so much the rights and wrongs of the science of HIV=AIDS as the mental framework which supports and sustains it. -TS

    Yes that is a great and important point. I have read for many people, Duesberg, The Perth Group, Harold Foster, Henry Bauer, and others, each presents a certain paradigm. Each author looks at it from a different perspective and breaks down the mainstream beliefs with different arguments and evidence. Deciding which framework to support will give one a headache. While some frameworks overlap with others, their multiplicity suggests that the problem has too many factors to justify the current mainstream method of studying, understanding, diagnosing, and treating “AIDS”.

  31. Truthseeker Says:

    Yes that is a great and important point. I have read for many people, Duesberg, The Perth Group, Harold Foster, Henry Bauer, and others, each presents a certain paradigm. Each author looks at it from a different perspective and breaks down the mainstream beliefs with different arguments and evidence. Deciding which framework to support will give one a headache. While some frameworks overlap with others, their multiplicity suggests that the problem has too many factors to justify the current mainstream method of studying, understanding, diagnosing, and treating “AIDS”.

    Anyone who describes what we write as a “great and important point” gets a free pass automatically here, but in this case we are not entirely sure that we are being understood in the way intended. A paradigm in an overarching belief or intellectual umbrella under which people operate as a group ie the belief that HIV is the cause of AIDS, and it is a shared premise which is not usually questioned by anyone in the group. I am not sure if any single author can be said to present an individual paradigm, but perhaps you are right. They certainly will tackle whatever topic they deal with by building a framework of ideas, and in the case of all the paradigm critics you mention, they (Harold Foster I am not familiar with) are all critics of a single paradigm, that HIV=AIDS. By definition they each offer an alternative paradigm, I guess, and these differ in various aspects, for example, the Perth Group seems to think that HIV doesn’t exist as an independent retrovirus, or anyway, hasn’t been shown to their satisfaction to be one, whereas Peter Duesberg believes it does and has been. It is hard to see what their alternative paradigm may be, but presumably it is the same as the one Duesberg is offering, the alternative belief that drugs, disease, malnutrition and stress are the causes of the immune collapse which is currently labeled as HIV=AIDS ie all ascribed to HIV. I don’t think it should give anyone a headache to agree with this. It is simply reverting to what one would think if Gallo had never been allowed to launch a fairy tale with federal backing. These factors have always impacted the immune system and always will.

    That Cal Crilly piece is rather good. It is an odd facet of the paradigm war over HIV=AIDS that musicians very often have much to contribute.

  32. Robert Houston Says:

    The appalling aspect of MIchael Specter’s New Yorker article was what he was praising. He seemed to be cheering on scientists who were attempting to revive past infections that once plagued the human race. Such attempts might be rationalized as contributing to basic research in pathogenesis but obviously hold the potential for perilous outcomes if the experiments go awry or the bugs get loose. Such efforts would appear to among the worst examples of sociopathic activities that are justified in the name of science. Let departed demons rest in peace.

    It’s hard to “detect the exit door to the HIV=AIDS global debacle opened by the presumably unwitting Michael [Specter] in this story,” as Truthseeker put it. For exogenous retroviruses to become tamed as endogenous ones may take many millenia. In sheep, the exogenous Jaagsickte retrovirus remains pathogenic even though it has an endogenous counterpart which is benign and even useful (K. Dunlap et al. Endogenous retroviruses regulate periimplantation placental growth and differentiation. PNAS 103(39):14390, 2006).

    Specter’s article ends with the views of Luis Villarreal, a scientist at UC/Irvine, who suggests that evolutionary selection for resistance to HIV “might take tens, or even hundreds, of thousands of years.” Villareal concluded, “If this were to be the outcome, we would see a new species of human marked by its newly acquired endogenous viruses.”

    That may be a way out of the “HIV=AIDS global debacle”, but who has the patience? Did the article anywhere indicate that such a process might be more rapid? And since HIV is generally admitted to be non-pathogenic for at least an average of 10 years after causing an initial brief cold in about half of its hosts, what would any of this matter? All the AIDS risk groups are subject to numerous possible immunosuppressive factors, of which HIV may be the least important – if indeed it plays any role at all.

  33. MacDonald Says:

    Specter’s article ends with the views of Luis Villarreal, a scientist at UC/Irvine, who suggests that evolutionary selection for resistance to HIV “might take tens, or even hundreds, of thousands of years.” Villareal concluded, “If this were to be the outcome, we would see a new species of human marked by its newly acquired endogenous viruses.”
    That may be a way out of the “HIV=AIDS global debacle”, but who has the patience? Did the article anywhere indicate that such a process might be more rapid?

    We can’t be certain when endogenous retroviruses entered our genome, because it is impossible to watch a five-million-year process unfold. Yet in Australia a retrovirus seems to be evolving in front of our eyes. Beginning in the late nineteenth century, koalas on the mainland were hunted nearly to extinction. To protect them, as many as possible were captured and moved to several islands in the south. In the past hundred years, those koalas have been used to replenish the population on the mainland and on several other Australian islands. In many cases, though, they have become infected with a retrovirus that causes leukemia, immune disorders, and other diseases. It can even kill them. The epidemic presents a significant threat to the future of the species, and scientists have followed it closely. One group, from the University of Queensland, looked for the virus in koala DNA—and, as one would expect with a retrovirus, found it. The team also noticed that some of the babies, known as joeys, were infected in the same locations on their DNA as their parents. That means that the virus has become endogenous. Yet, when the scientists examined the koalas on Kangaroo Island, in the south, they discovered something they had not anticipated: none of the koalas were infected.
    That could mean only one thing: since the infected animals had all been moved just in the past century, the koala retrovirus must have spread to Australia recently and is entering the genome now.

  34. Truthseeker Says:

    Did the article anywhere indicate that such a process might be more rapid? – Robert Houston

    Where does it say that any line of claim or theory issuing from the castle on top of the HIV=AIDS hill has to be scientifically sensible and in line with what we thought we already knew about retroviruses, viruses, human disease and immunity? You haven’t noticed that over 23 years the theorizing attached to this meme rarely if ever accords with what history and practice indicates? This is the marvelous aspect of HIV=AIDS, that it is almost entirely unmoored from reality and science proper, and all involved are free to fashion almost any kind of fantastic addition to the prevailing corpus of ‘knowledge’ in any direction they please, as long as it fulfills the two inviolable principles of HIV=AIDS theorizing, which is that a) it does not explicitly contradict the premise that HIV causes AIDS, however inconsistent it might be with that dogma and b) it demands that further large sums be spent on HIV=AIDS research and development.

    What we are discussing here is the future of the grand propaganda exercise that sustains and spreads the HIV=AIDS meme. If the actual evidence discovered by studies continues to show ever more clearly that HIV does not and never has caused AIDS on any level other than panic and terror, the strain between fantasy and fact will eventually force an accommodation of some kind, as the gap between facts and belief widens to an intellectual Grand Canyon. To a seasoned propagandist such as the typical leader of HIV=AIDS paradigm belief in the NIAID, Harvard, Cornell and elsewhere, this presents no particular problem. Just fantasize in some direction novel to the press and public and it will be another few years before they catch up and the gap between sense and nonsense becomes visible through the fog once again.

    Science is science and propaganda is propaganda but no one in HIV=AIDS has the slightest difficulty in cooking both in the same pot.

  35. Nick Naylor Says:

    TS, you said, “Rezaf, the great absurdity about this whole scene is how difficult it is for people to comprehend that the whole deal was a piece of nonsense from the word go.”

    But let me submit that you’ve misread the Specter piece, not considering that it is a mixture of good science journalism and nonsense. In other words taking the sharp red pencil to the nonsensical HIV parts leaves us with an excellent overview of the state of research into endogenous retroviruses.

    “To change the belief you have to change the framework.”

    Exactly. And this is precisely how we can use the correct parts of the Specter peace.

    MacDonald says, “The predictable answer from HIV enthusiasts will of course be that attacking this key control mechanism is just one, therefore not necessarily sine qua non, among the endless number of ways the endlessly resourceful, endlessly multi-tasking, endlessly mysterious tiny piece of unremarkable RNA accomplishes its deadly purpose. The HIV-AIDS hypothesis is, in other words, endlessly unfalsifiable.”

    That’s it. This is precisely how they keep the paradigm going and why WE should move beyond the catch-phrase “harmless passenger virus”.

    Also (MacDonald), “Martin Kessler and the rest, Dr. Maniotis has solved the linguistic problem for us. What is called HIV in orthodox-speak is now called a ‘molecular signature’ in rethinker-speak. We acknowledge that a molecular signature is registered, but we suspend judgement as to what signed, where it came from and what it means.”

    I’m still amazed that our A-team dissident scientists can’t come together on this.

    And TS, you then respond, “In other words, MacD, if you would, hew to the grand tradition of NAR and spell everything out so even the likes of the humble host can follow it, otherwise there is no hope of getting the message across to the HIV faithful if they come here to learn from their betters.”

    Aaarrgggh … do you have to play THIS CARD at this CRITICAL MOMENT? Don’t you see from recent news that the HIV establishment FULLY COMPREHEND, one could even say they’ve co-opted the MacDonald/Naylor critique.

    You then add insult to injury with (to MacDonald), “The dear host does not know what the heck you are talking about. Is there some law on the planet you speak from which forbids saying straightforwardly, like a real man, what your point is, that the paper proves to your satisfaction, which Rezaf agrees with”

    You write this long-winded essay on the Specter piece and then once again go mickey mouse with the feigned incomprehension bit – you’re all purpose defense against the valid science of endogenous retroviruses? And you make a crack about being a “real man”??!! What the F*** is this supposed to add to the discussion?

    Robert Houston has constructively redirected this thread to a critical analysis of certain parts of the Specter piece. So let’s move forward on that basis, TS. You can help by not insisting on this ridiculous admonition that everything needs to be reduced to “sound-bytes”. The HIV sound-bytes are precisely what destroy the credibility of Specter’s otherwise good science journalism.

  36. Nick Naylor Says:

    Let me add that Villareal is a mixed bag that illustrates why outsiders are necessary to restore science to this inbred community.

    His comments on what is also called “horizontal gene transfer” in evolution are spot on.

    His predictions for Africa are the worst kind of unvalidated scare-mongering but after all, he produced an excellent sound-byte.

  37. Truthseeker Says:

    The expression is “sound bite”, Nick, I believe. And the point of asking you and McD to explain yourselves to the world like real men ie grasping what you have to say firmly enough that it doesn’t slip from the clutch of those less clever than yourselves as you hand them your torch of truth, is that the world has little patience for challenging and novel ideas and you can only get such points across to the world by making them clear, as the editors of the New Yorker have long known, and which is if you will forgive us saying so actually the only proof that you have anything to contribute, since obscurity can veil nonsense in the same camouflage as sense.

    I am glad you think that the non HIV parts of the Specter essay make sense and that you think they can be turned to advantage by those who wish to replace the HIV=AIDS paradigm. Until you can express your perception as to how this is possible in words of two or even one syllable, however, I am afraid the ordinary gaping admirer of your brilliance such as your long suffering host is going to be left in the dark.

    I am not in any way hostile to the science of endogenous retroviruses and for all I know of the matter maybe most of our junk DNA is made up of such elements, and they may be of great importance in the scheme of things in ways we have yet to discover, and possibly the number of retroviruses which are exogenous may be minimal by comparison, or whatever, that is not the point here.

    For we are not reading Specter’s piece with any great faith in it as a guide to science we can count on while he is in the hands of people who accept the long exploded premise that HIV causes AIDS, and neither he nor they are people we can count on for guidance until this misunderstanding is banished from the assumptions they are working on, whether it is directly involved or not.

    That is the problem with the whole field, and one which we are trying to solve in our modest way by insisting on the correction. If you can produce anyone involved who is willing to repudiate HIV=AIDS publicly we would be glad to trust their other perceptions about the reality of the world of retroviruses, but not otherwise. We certainly don’t trust anything that Specter writes on the topic. It is rather like expecting Samantha Powers to give us the correct analysis of what is really going on in the Sudan. None of these people has any credit in our book, as long as they are taken in by this prima facie absurd claim.

    That is why it is incumbent on you to make perfectly clear what it is you are trying to say, so that even I can understand it, and know what it is in Specter’s account that you agree with and support and confirm. Please feel free to be long winded if that is necessary to do the job.

  38. yello Says:

    (Jaw drops) O.MY.GOD.

    Experts call for rethinking AIDS money

    By MARIA CHENG, AP Medical Writer
    Fri Jan 18, 12:38 PM ET

    LONDON – In the two decades since AIDS began sweeping the globe, it has often been labeled as the biggest threat to international health.

    But with revised numbers downsizing the pandemic — along with an admission that AIDS peaked in the late 1990s — some AIDS experts are now wondering if it might be wise to shift some of the billions of dollars of AIDS money to basic health problems like clean water, family planning or diarrhea.

    “If we look at the data objectively, we are spending too much on AIDS,” said Dr. Malcolm Potts, an AIDS expert at the University of California, Berkeley, who once worked with prostitutes on the front lines of the epidemic in Ghana.

    Problems like malnutrition, pneumonia and malaria kill more children in Africa than AIDS.

    “We are programmed to react quickly to small children with AIDS in distress,” Potts said. “Unfortunately, we don’t have that same reaction when looking at statistics that tell us what we should be spending on.”

    The world invests about $8 billion to $10 billion in AIDS every year, more than 100 times what it spends on water projects in developing countries. Yet more than 2 billion people do not have access to adequate sanitation, and about 1 billion lack clean water.

    In a recent series in the journal Lancet, experts wrote that more than one-third of child deaths and 11 percent of the total disease burden worldwide are due to mothers and children not getting enough to eat — or not getting enough nutritional food.

    “We have a system in public health where the loudest voice gets the most money,” said Dr. Richard Horton, editor of Lancet. “AIDS has grossly distorted our limited budget.”

    But some AIDS experts argue that cutting back on fighting HIV would be dangerous.

    “We cannot let the pendulum swing back to a time when we didn’t spend a lot on AIDS,” said Dr. Kevin De Cock, director of the AIDS department at the World Health Organization. “We now have millions of people on treatment and we can’t just stop that.”

    Still, De Cock once worked on AIDS projects in Kenya, his office just above a large slum.

    “It did feel a bit peculiar to be investing so much money into anti-retrovirals while the people there were dealing with huge problems like water and sanitation,” De Cock said.

    Part of the issue is advocacy, from celebrity ambassadors to red ribbons.

    “No one is beating the drum for basic health problems,” said Daniel Halperin, an AIDS expert at Harvard University’s School of Public Health.

    Aside from southern Africa, most of the continent has relatively low rates of HIV, and much higher rates of easily treatable diseases like diarrhea and respiratory illnesses. Yet much of the money from the West, especially from the United States, goes into AIDS.

    Halperin recently wrote a commentary in The New York Times on the imbalance and said he was astounded by the response. Most were positive, he said, with many AIDS experts agreeing it was time to re-examine spending.

    Most AIDS officials say the solution is to boost the budget for all of public health.

    “Why does the public health budget have to be so limited?” asked Tom Coates, a professor of global AIDS research at the University of California, Los Angeles. “Let’s not drag AIDS care and prevention down to the level of every other disease, but let’s bring everything else up to the level of AIDS.”

    That may be wishful thinking.

    “At the end of the day, there are limits to how big the public health pie can be,” Halperin said.

    Since the discovery of anti-retrovirals to fight HIV in the 1990s, AIDS has virtually become a chronic, treatable disease in the West. But the disease has not been conquered so easily in Africa. Not only are the AIDS drugs too expensive for most patients, but major problems in the health system need to be fixed first.

    “It’s hard to get Western donors to listen,” said Dr. Richard Wamai, a Kenyan doctor at Harvard’s School of Public Health.

    Wamai said that some African health systems are so weak they cannot absorb the donations, and AIDS drugs are sometimes left in warehouses because governments cannot distribute them.

    Still, “trying to redirect AIDS money will take a long time,” Wamai said. “It’s a bit like trying to stop an ocean liner.”

    http://news.yahoo.com/s/ap/20080118/ap_on_he_me/rethinking_aids_1;_ylt=Amy35zzRg1CUtYEmPMlap3Va24cA

Leave a Reply

You must be logged in to post a comment.


Bad Behavior has blocked 2855 access attempts in the last 7 days.