Six Questions On The HIV-AIDS Hypothesis
Dean
Discussions began here on Dean's World last week on the topic of researchers, physicians, and people who are diagnosed HIV+ who question whether HIV causes AIDS. Discussion has raged on the question ever since. This week has been no exception.
In response to those discussions, I recently received the following email from Dr. Harvey Bialy. Bialy is scholar-in-residence and coordinator at the Institute of Biotechnology, UNAM. He was the founding scientific editor of, and then became Editor-at-Large for, Nature Biotechnology. He was a member of the Presidential Advisory Panel on AIDS in South Africa. He is most recently the author of Oncogenes, Aneuploidy, and AIDS: A Scientific Life and Times of Peter H. Duesberg, of which you can read a sample chapter here. His letter is as follows. --Dean
Dean,
As the answers to all of the questions contained in the comments from your visitors can easily be found in the literature, I prefer instead to ask some questions of my own, and if they can provide me with answers to all or any of the following, I would be delighted. I have sought in vain in the scientific literature on HIV/AIDS (a literature that now numbers more than 130,000 peer-reviewed publications) for such answers, as have Profs. Duesberg, Gilbert, Mullis and others. But they should not feel badly if they cannot answer them either, since neither could Drs. Baltimore, Fauci, Gallo, Montagnier, Weiss and others when they were posted on President Thabo Mbeki's AIDS Advisory Panel's intranet discussion in June of 2000. In fact, the inability to answer these and numerous other questions was what prompted the emergency call to religious fervor embodied in the notorious Durban Declaration.
I am eager to read what your clever and earnest readers stroke.
Harvey
Editor's note: In the interim between receiving the email above and this posting, I received the following from Dr. Bialy. --Dean
PS: Use of the NIH website, which was created expressly for the purpose of being able to say that the "Duesbergian" arguments have been amply refuted, is disallowed because this annonymous web document, exactly like the Durban Declaration, references its conclusions with papers that themselves only restate the assertions rather than offer the proof of them. It is really a pathetic document, and numerous attempts by Peter (Duesberg), David (Rasnick), and myself to get someone at the NIH to put their name to it so that its contentions could be further debated have been unsuccessful.
Six fatal inconsistencies in the virus-AIDS hypothesis
I respectfully request that one or more members of the panel provide concise answers, with references, to the six question sets below. I am especially interested to obtain an answer to the overall question as to why the uncontested, published data to which I refer does not cast any doubt on the hypothesis that the T4 cell depletion characteristic of AIDS patients, and which presumably leads to their deadly opportunistic infections, is due to a new, mutant retrovirus, known since 1985, as HIV.
Given that all current treatment and prevention efforts are based entirely on this hypothesis, its validity must certainly be establish able beyond any reasonable doubt. Competing hypotheses are the hallmark of science, and in another discussion group Drs. Duesberg andRasnick will provide material relevant to an alternative explanation for the collective epidemiological, microbial, chemical and medical phenomena that are called AIDS. Here I am concerned to ha ve it clearly established as to exactly why the following accumulation of published data concerning HIV do not persuade those who hold that HIV is a pathogen to acknowledge its characteristic passenger virus epidemiological behavior, genetics, and biochemistry.
Specifically:
1. Why has not a single chimpanzee, out of more than 250 successfully infected since 1984, developed AIDS? There is not one other human viral pathogen that cannot reproduce a similar disease in chimps (Duesberg, P.H., Pharmacology & Therapeutics 55: 201-277, 1992). Arguments concerning simian viruses and simian AIDS are not relevant. As pointed out at great pains in the above review article, these animal diseases are not suitable models of human AIDS. (Note for the skeptical: the editor of this journal, Dr. David Sugar, (shugar@xxxx.edu.pl) has on file literally hundreds of pages of the most extraordinarily detailed review process that this paper underwent before publication.)
I would, in the light of the apparent openness of some of you to now consider previously unacknowledged arguments, and a renewed interest in defending your well-fortified hypothesis in the best tradition of science, offer the following correlative of the chimp infection data. The passenger-HIV hypothesis, as opposed to the pathogenic-HIV one, predicts that "viral load" measurements on infected chimps over time show precisely the same fluctuations as measurements made using sera obtained from infected humans (whether "medicated" or not). Any takers?
In the event that the question about the chimps is dismissed with some flippancy such as "there is always something new under the sun," then I would at least expect a direct reply to the following, related question. Why do the large numbers of US long-term (10-15 + years), "medication"-free survivors of their AIDS diagnosis not require that the HIV=Death "equation" be rewritten? The clearest documentation of this claim can be found in the appendix of C. Maggiore, What if Everything You Thought You Knew About AIDS Was Wrong? (The American Foundation for AIDS Alternatives, ISBN 0-9674153-0-6, 2000) in which she reproduces over 50 sworn testimonials of the hundreds on file with her organization.
2. Why do the in vivo and in vitro virus neutralizing antibodies that are present in easily assayable amounts in the blood of HIV infected people (Daar, E.S., Moudgil, T., Meyer, R.D. and Ho, D.D. (1991) New Engl. J. Med. 324: 961-964) not protect against AIDS if HIV is the culprit? I trust that the tragically data-less graph that shows "theoretical" increases and decreases in viral antigens, viremia, neutralizing antibodies and T cells is not brought up. Its well documentable history is too embarrassing for you to possibly want it posted here. A related question is why Pneumocystis carinii pneumonia is not the most common AIDS defining disease across all demographic and geographic spectra since it is a 100% ubiquitous latent human pathogen? (Pifer, L.L. (1984) Eur. J. Clin. Microbiol. 3: 169-173).
3. Why is the incidence of HIV in the US population constant over 20+ years (US Centers for Disease Control HIV/AIDS Surveillance, Year -end editions since 1984) if the virus and disease are new and epidemic? This clear violation of Farr's Law of epidemiology must be addressed unambiguously, as it is absolutely relevant to the question of the presumed African heterosexual epidemic.
4. Why has every attempt to detect an actual viremia that is consistent with a pathogenic role for HIV failed? In this regard, I would expect that someone will defend the biochemical marker measurement known as "viral load" as something resembling an accurate measure of infectious virus.
5. What is there in the genetic structure or organization of HIV that distinguishes it functionally from other retroviruses such as HTLV-I and II that are not said to cause AIDS?
The citing of apparently different orfs in these viruses is not convincing since a functional genomic analysis can produce similar orfs for almost all of the human and animal retroviruses with sequences deposited in GenBank (G. Moreno and J. Collado, Bioinformatics Unit, International Center for Nitrogen Fixation, UNAM, analysis available on request). Corollaries of this are (a) why has no AIDS-specific gene or genes been identified despite an accumulated research expenditure that amounts to more than one million dollars US per nucleotide, and (b) since all genes of HIV are essential for replication (Duesberg, P.H. (1989) Proc. Nat. Acad. Sci. U.S.A. 86: 755-764), and there is no possibility of differential transcription from an integrated retroviral genome (Ibid), any postulated AIDS-gene would be expected to function during primary acute infection when there is detectable virus transcription and replication, and thus cause AIDS immediately not 10 years later when the virus is restricted to a few cells and is not making RNA in more than 1 in 1000 of those at any given time (Harper, M. E., Marselle, L. M., Gallo, R. C. & Wong-Staal, F. PNAS 83: 772-776 (1986), Simmonds, P., et al. J. Virol. 64: 864-872 (1990), Pantaleo, G., et al. Nature 362: 355-358 (1993).
6. Why are exactly the same cells that HIV is said to kill in vivo not killed in vitro where productively infected cultures continue to produce 1000s of infectious particles per day for use in the various "AIDS tests' and are not protected by antibodies or 'antiretroviral' drugs (although they are by patents)?
Dr. Bialy contends that today, nearly five years later, no one has successfully answered any of the above questions, that none of them are "trick questions," and that instead of answering these questions an apparently panicked AIDS establishment produced the Durban Declaration instead. You can read the Durban Declaration by clicking here. You will also probably want to read The Durban Declaration Is Not Accepted by All, which was published in Nature in September 2000 but is not, apparently, available on their web site.--Dean)
All Related Posts (on one page) | Some Related Posts:
Dr. Bialy: Some would say that you are merely a tenured professor and are not a front-line physician involved in treatment, and you have relatively few peer-reviewed articles on AIDS to your credit, at least from a preliminary search through Medline. Perhaps one might even say that you have the luxury of sitting back and poking holes in others' work without having to actually put forth original research of your own.
This may seem like a softball question, but: why should we take you seriously?
Anyway, my "reasonable speculation":
(I don't know enough to even understand #4)
"Why has not a single chimpanzee, out of more than 250 successfully infected since 1984, developed AIDS?"
Maybe because HIV comes from chimps and has evolved in chimps to be relatively harmless as viruses often do in their usual hosts.
A good question, but there's too many unknowns for me to consider it a "fatal" question.
"Why do the in vivo and in vitro virus neutralizing antibodies that are present in easily assayable amounts in the blood of HIV infected people (Daar, E.S., Moudgil, T., Meyer, R.D. and Ho, D.D. (1991) New Engl. J. Med. 324: 961-964) not protect against AIDS if HIV is the culprit?"
Because life isn't always that easy?
I mean, there are other lethal pathogens in the world. Do none of them induce antibody production? I always thought that they did, but maybe I'm wrong. I'd like you to tell me, because I think it's a bit unfair to ask me to acquaint myself with the literature of diseases besides AIDS, too :)
"A related question is why Pneumocystis carinii pneumonia is not the most common AIDS defining disease across all demographic and geographic spectra since it is a 100% ubiquitous latent human pathogen?"
I would guess that a severely weakened immune system is not a non-existent one, so that the risk of infection grows, but not to 100%. It seems to me that infections are normally like that. You're either sick or you're not. You don't get half sick.
"Why is the incidence of HIV in the US population constant over 20+ years (US Centers for Disease Control HIV/AIDS Surveillance, Year -end editions since 1984) if the virus and disease are new and epidemic?"
Farr's law seems like a crude generalization which I never would have expected to be true all the time. I'm sure even slightly changing a few parameters could lead to a completely different curve. A lot of diseases seem to hold relatively steady, but I guess they aren't "epidemics". Does that matter?
"What is there in the genetic structure or organization of HIV that distinguishes it functionally from other retroviruses such as HTLV-I and II that are not said to cause AIDS?"
That's a pretty hard question (I don't understand why there has to be a specific "AIDS gene", as opposed to a more holistic effect). So if biologists don't know, that doesn't strike me as much of a failure.
"Why are exactly the same cells that HIV is said to kill in vivo not killed in vitro where productively infected cultures continue to produce 1000s of infectious particles per day for use in the various "AIDS tests' and are not protected by antibodies or 'antiretroviral' drugs (although they are by patents)?"
It certainly wouldn't be the first thing that works only in vivo.
Is it just me, or do those questions look like they'd make great Doctoral dissertations (I Am Not An Academic) or be good things for NIH to spend money on (I Am Not A Medical Professional)?
Even if HIV does cause AIDS, the answers to those questions look to this rank amateur like they could easily lead to viable vaccines or treatments.
1. Knowing why HIV doesn't give chimps AIDS could either prove HIV doesn't cause AIDS, or help us develop a vaccine or treatment by allowing us to imitate what the chimps's bodies are doing.
2. Knowing why the antibodies don't prevent AIDS could either prove HIV doesn't cause AIDS, or help us develop a vaccine or treatment by producing a vaccine which provokes a better antibody, or by defeating whatever mechanism HIV uses to protect itself from the antibody.
3. Knowing why HIV is epidemic in Africa and not America could either prove HIV doesn't cause AIDS, or help us slow or stop the epidemic in Africa by exporting our methods to Africa.
4. Knowing why we can't find enough HIV in the bloodstream to consider it pathogenic could either prove HIV doesn't cause AIDS, or help us develop a vaccine or treatment.
5. Knowing functional genetic differences between HIV and other retroviruses could either prove HIV doesn't cause AIDS, or help us develop a vaccine or treatment.
6. Knowing the difference between in vivo and in vitro could either prove HIV doesn't cause AIDS, or help us develop treatments.
My point that I tried to make before and failed is that, in cases where a capable and conscientious scientist takes a dissenting view to a current consensus theory, investigation into that dissent is good science and will have fruitful results, even if the consensus view is proved correct. Why? One reason is that capable and conscientious dissenting scientists ask such fantastic questions. All this supports Dean's continued contention that scientific dissent should be encouraged, not suppressed.
Side note: why do people act like understanding science is difficult and that the public can't make good collective decisions based on science? Doing science is hard, creative work. Understanding science is something everyone with an average IQ should be able to do. Just like wrting symphonies is hard creative work. But understanding and responsding to them is something most of us can do. Of course I've probably misunderstood at least one of these questions in some fundamental way. If I have, remember my rank amateur status.
Yours,
Wince
My answer to #1 is to ask him how many humans infected with SIV have become sick? There are innumerable examples of viruses that don't cross the species barrier, even between humans and other primates (eg. Ebola Reston). Just because our DNA is >99% identical doesn't mean that humans and chimps respond the same to all insults. I'm sure that I would test positive for rodent viruses that I have been exposed to in my research, but I don't have any symptoms, and I'm not likely to, either.
As for #2, anyone who has studied immunology knows that antibodies work by "tagging" invaders for later destruction. If the destruction system is failing (the very cells attacked by HIV), the antibodies can do all they want. It's as if a crew of lumberjacks tagged all the trees on a plot of land to be cut down, but the sawyers were prevented from doing the subsequent cutting. As to the PCP argument, patient condition and background genetics plays an EXTREMLY important role in the susceptibility to any disease, and we don't know yet what other factors are involved in contracting PCP, including genetics, stress level, nutrition, etc.
#3 As I recall, Farr's law assumes a static population, but even if this is not the case, the interaction of mitigating factors (drugs, nutrition, etc) and population dynamics could account for the changes. If you look at world AIDS numbers, it would seem we are still in the rising phase of the epidemic.
#4 I suspect that the answer to this question has to do with the biases of the questioner as to what level of viremia qualifies since viral load is probably best described as an approximate measure, correlative but not quantitative.
#5 isn't a fair question. This research is ongoing, and if we can't tell how each individual's genome is responsible for our inter-individual (not to mention inter-species) differences, it's not reasonable to ask the same question about viruses which are approximately the same % different from each other.
And as for in vivo/in vitro comparisons, a first year biosciences PhD student could destroy that question. maor is absolutely right. There is no question that in vitro analysis is a poor substitute for in vivo answers. There are too many factors that are missing in the dish.h
And you can blame any logic faults (above)on my awful head cold
What would, in your mind(s), disprove or at least greatly diminish the theory?
I have no stake in either the HIV = AIDs theory or its negative, but I have usually found asking for reasonable falsifying scenarios edifying.
Do I sense that there is a problem in that the mortality of Africa is really not any different from what it had been before "HIV-AIDS"? Despite the fact that the medical establishment has been saying for years that without billions in (mostly American) money Africa would cease to exist as a functioning modern society, because of "HIV-AIDS"? If, that is, one conceives that it has ever existed as a functioning modern society.
No one here is going to shoot off quick answers to any of this. These are the questions he posed before the symposium of the world's top AIDS scientists in 2000. Many of the foremost experts in the world of AIDS research were there--and none of them had a response to any of thse questions.
Instead they issued the Durban declaration and congratulated themselves.
Some of Dr. Bialy's questions may indeed be thesis sized but it's disturbing that in 20 years of research that these are unanswered questions.
First: Dean's softball question:
Dean,
I thought we both made it pretty clear that I was to evaluate answers, not take further questions, of which I have a surfeit of my own. Nonethesless, I will answer you, and only you, this one time.
You ask "Why should we take you seriously?"
1. The question is more properly addressed to youself, since you are the instigator of your high-ranking power blog's interest in my "armchair" opinions, and the one who posted the question set and its introductory caveats. I think that you have actually made it abundantly clear why you take me and Duesberg and other "AIDS insurgents" seriously. Thus I can only conclude that you were indeed lobbing a "softball" for the purposes of getting some other balls rolling.
2. The basic compositional premise of "Oncogenes, Aneuploidy and AIDS" is "res ipsa loquitur" (the thing speaks for itself). The question set does likewise and requires no further authority.
Now on to "the beef", as a popular television advertisement featuring a feisty old lady once had it. OK?
Maor,
Your attempts at answers are by your own admission "speculation". The data I presented are not speculative. Your inability to provide reasoned, properly referenced answers, coupled with your very obvious ability to run off at the mouth at a moment's notice earns you an F.
So as you do not think me a total bastard. I will give you two corrections of your hand-waving answers.
You write in answer to question abt PCC pneumonia:
""A related question is why Pneumocystis carinii pneumonia is not the most common AIDS defining disease across all demographic and geographic spectra since it is a 100% ubiquitous latent human pathogen?"
I would guess that a severely weakened immune system is not a non-existent one, so that the risk of infection grows, but not to 100%. It seems to me that infections are normally like that. You're either sick or you're not. You don't get half sick."
The answer requires much more than guessing, and even so misses the point of the question entirely. It is a question about frequencies not absolutes.
2. ""Why do the in vivo and in vitro virus neutralizing antibodies that are present in easily assayable amounts in the blood of HIV infected people (Daar, E.S., Moudgil, T., Meyer, R.D. and Ho, D.D. (1991) New Engl. J. Med. 324: 961-964) not protect against AIDS if HIV is the culprit?"
Because life isn't always that easy?
I mean, there are other lethal pathogens in the world. Do none of them induce antibody production? I always thought that they did, but maybe I'm wrong."
You need to educate yourself on what a neutralizing antibody is. Viral diseases in which antibodies do not protect are characterized by rapid replication of the pathogen which outpaces the two weeks or so required to mount an effective immune response. The reason most viral diseases disappear after a while without killing us is that the infecting agent is eventually overcome by the immune system and the amount of virus reduces to near zero. In the case of HIV and AIDS this fundamental observation is turned upside down. There is plenty of virus neutralizing antibody at all times and there is precious little virus ever. Yet HIV is said to be pathogenic.
I'm not sure if you are one or two as your comment allows for both possibilities, although I think you are a singular, and I hope not
unique being, at least in your thinking.
Whether one or two, my time was far from wasted by reading your intelligent and thoughtful comment. I could not agree more with your
analysis.
I would only add, that the absolute inability by the most prominent AIDS researchers to provide defensible answers to these questions (I refer again to the fallback Durban "Declaration") more than favors the passenger virus hypothesis.
I hope you will read my book, and even give me some feedback.
Harvey
Grade F.
1. My answer to #1 is to ask him how many humans infected with SIV have
become sick? THE QUESTION IS ABOUT CHIMPS AND HIV. IT EXPLICITLY
EXCLUDES SIV. There are innumerable examples of viruses that don't cross
the species barrier, HIV PRODUCTIVELY INFECTS CHIMPS. THUS IT DOES CROSS
THE SPECIES BARRIER. even between humans and other primates (eg. Ebola
Reston). Just because our DNA is >99% identical doesn't mean that humans
and chimps respond the same to all insults. EVERY OTHER HUMAN VIRAL
PATHOGEN CAUSES A SIMILIAR DISEASE IN CHIMPS AS EXPLICITLY STATED IN THE QUESTION I'm sure that I would test
positive for rodent viruses that I have been exposed to in my research,
but I don't have any symptoms, and I'm not likely to, either. YOU ARE
NOT A CHIMPANZEE AND YOU HAVE NOT ACCIDENTLY BEEN INFECTED WITH A HUMAN
VIRUS.
As for #2, anyone who has studied immunology knows that antibodies work
by "tagging" invaders for later destruction. If the destruction system
is failing (the very cells attacked by HIV), THE NEUTRALIZING AB TAGS
THE VIRUS INDEED, AND IT IS INDEED DESTROYED. AN AB-COATED VIRUS CANNOT CONTACT THE CD4 OR ANYOTHER RECEPTOR AND WILL EVENTUALLY BE CONSUMED BY PHAGOCYTIC CELLS...NOT T CELLS.THIS IS WHY THERE ISN'T
ANY MEASURABLE INFECTIOUS VIRUS IN AIDS PATIENTS, EXCEPT OCCASIONALLY AS WITH ALL OTHER PASSENGER INFECTIONS. SO THE QUESTION AS TO HOW NEGLIGIBLE VIRUS KILLS MILLIONS OF CELLS REMAINS UNANSWERED TO THIS DAY DESPITE MORE THAN 50
BILLION RESEARCH DOLLARS IN TRYING! IT IS BEYOND THE PALE THAT YOU CLAIM NO FUNDS FOR THIS RESEARCH AT THE BOTTOM OF YOUR POSTthe antibodies can do all they want. ( AS A FRIENDLY OLD PROFESSORIAL ASIDE: CEASE USING ANTHROPOMORPHIC LANGUAGE WHEN ATTEMPTING TO THINK ABT BIOCHEMISTRY) It's as if a crew of lumberjacks tagged all the trees on a plot of land
to be cut down, but the sawyers were prevented from doing the subsequent
cutting.THIS IS A NICE ANALOGY BUT IT IS NOT AN ACCURATE ONE. A BETTER ANALOGY IS THAT THE TREES ARE TAGGED WITH SOMETHING THAT MAKES THEM STOP GROWING. THIS IS WHAT A NEUTRALIZING ANTIBODY DOES (IT STOPS FURTHER REPLICATION) SO NO TREE CUTTERS ARE REQUIRED. YOU ARE GETTING AB MEDIATED CYTOLYSIS CONFUSED WITH AB MEDIATED NEUTRALIZATION, WHICH CAN, BUT DOES NOT NEED TO, INVOLVE WHITE BLOOD CELLS THAT ARE NOT PREFERENTIALLY INFECTED BY HIV. AND REMEMBER THAT ONLY A SMALL FRACTION OF SUSCEPTIBLE T CELLS ARE EVER INFECTED. YOU MIGHT LIKE THIS ANALOGY. CLAIMING THAT HIV KILLS THE T CELL ARM OF THE IMMUNE SYSTEM IS EQUIVALENT TO SAYING THAT THE AMOUNT OF BLOOD SOMEONE LOSES IN CUTTING THEMSELVES SHAVING EVERYDAY GIVES THEM ANEMIA. I As to the PCP argument, patient condition and background
genetics plays an EXTREMLY important role in the susceptibility to any
disease, and we don't know yet what other factors are involved in
contracting PCP, including genetics, stress level, nutrition, etc.
THIS IS A QUESTION ABT FREQUENCIES DEAR. PCC IS THE MOST COMMON LATENT
PATHOGEN ... 100% SO. THUS PCCP SHOULD BE STATISTICALLY THE MOST COMMON AIDS
DISEASE REGARDLESS OF BACKGROUND. IT IS NOT. THIS ONLY HIGHLIGHTS THE
ARBITRARY WAY AIDS DISEASES ARE ASSIGNED. LIKE THE WAY CERVICAL CANCER
BECAME AN AIDS DISEASE BECAUSE OF DISABILITY CONCERNS, NOT SCIENTIFIC
ONES.
3. #3 As I recall, YOU ARE UNBELIEVABLY PRESUMPTUOUS. FIRST PASS? LOOK
DAVID BALTIMORE THE PRESIDENT OF YOUR UNIVERSITY ..ALTHOUGH NOONE
INCLUDING JIM WATSON KNOWS HOW THAT CAME TO BE...COULD NOT ANSWER THESE.
Farr's law assumes a static population,THE US POP IS RELATIVELY STATIC AT 250 MILLION OVER THE PAST 20 YEARS but even if this is not thecase, the interaction of mitigating factors (drugs, nutrition, etc) and population dynamics could account for the changes. If you look at world
AIDS numbers, it would seem we are still in the rising phase of the
epidemic. THESE FACTORS CANNOT EFFECT A GENERAL POPULATION WIDE EPIDEMIC, WHICH IS WHAT AIDS HAS BEEN SAID TO BE...REMEMBER...EVERYBODY IS AT RISK...IT IS EVERYBODY'S DISEASE, EVEN THOUGH BOTH OF THESE ARE OBVIOUSLY UNTRUE. LOOK, THIS IS EXACTLY A STATISTICAL ARGUMENT. MILLIONS OF TESTS...OVER 20 YEARS ...FLAT LINE. ONLY ONE CONCLUSION POSSIBLE. OLD VIRUS. UNFORTUNATELY THIS IS HOW AIDS CASES ARE REPORTED. BUT IT IS INCORRECT.
TO HAVE AN EPIDEMIC YOU HAVE TO HAVE MORE CASES IN YEAR A THAN IN YEAR
A-1. THIS HAS NOT BEEN TRUE FOR AIDS IN THE US SINCE 1985 OR SO.
#4 I suspect that the answer to this question has to do with the biases
of the questioner as to what level of viremia qualifies since viral load
is probably best described as A SPECIOUS AND MISLEADING TERM THAT DOES NOT CONVEY WHAT IT MEANS AT ALL, WHICH IS THE CORRELATION BETWEEN PCR CYCLES AND THE ORIGINAL AMPLICON...A CORRELATION THAT IS MEANINGLESS IF TRYING TO INFER INFECTIOUS VIRUS FROM IT. an approximate measure, correlative but
not quantitative. YOUR SUSPICION IS NOT AN ANSWER. IF YOU READ BEFORE
RUNNING OFF AT THE MOUTH YOU WOULD KNOW EXACTLY WHAT LEVELS I AM
REFERRING TO. 1.7 OR SO INFECTIOUS PARTICLES, NOT PCR UNITS, PER ML OF
SERUM. NADA CLINICALLY FOR ANY VIRUS AT HOMEOSTASIS.
#5 isn't a fair question. This research is ongoing,NO IT ISN'T. IT IS A
DONE DEAL IT MIGHT HELP IF YOU READ THE ENTIRE QUESTION BEFORE TRYING TO ANSWER IT FROM YOUR OBVIOUSLY VAST PERSONAL KNOWLEDGE BASE. THE VIRUS HAS A GENETIC COMPLEXITY OF 9 KB. IT HAS BEEN ANALYZED TO DEATH. THERE IS NOTHING TO DISTINGUISH IT FUNCTIONALLY FROM
ALL OTHER RETROVIRSUES THAT ARE NOT SAID TO CAUSE AIDS. NOTHING MORE TO
SAY DEAR. and if we can't tell how each individual's genome is
responsible for our inter-individual (not to mention inter-species)
differences, it's not reasonable to ask the same question about viruses
which are approximately the same % different from each other. THESE ARE
PRECISELY THE QUESTIONS THAT DROVE THE HUMAN GENOME PROJECT BUT A COMPLEXITY OF SEVERAL BILLION IS ANONGOING ANALYSIS. NOT SO 9 KB. BTW FUNCTIONALLY IMPORTANT INTERSPECIES DIFFERENCES ARE EASY TO SPOT IN A PROPERLY CONDUCTED BLAST OR OTHER GENOMIC ANAYLSIS, INDIVIDUAL DIFFERENCES ARE NEXT TO IMPOSSIBLE FOR EVEN SIMPLE ORGANISMS. GOT IT.?!
And as for in vivo/in vitro comparisons, a first year biosciences PhD
student could destroy that question. maor is absolutely right. There is
no question that in vitro analysis is a poor substitute for in vivo
answers. There are too many factors that are missing in the dish. ONCE
MORE YOU MIX THINGS UP. LOOK WHEN IN VIVO AND IN VITRO DON'T MATCH IT IS
ALMOST ALWAYS THAT THE IN VITRO RESULT (CANCER FOR EXAMPLE) IS NOT
REPRODUCED IN VIVO NOT THE OTHER WAY AROUND. THINK. YOU HAVE NAKED,
UNPROTECTED CELLS IN CULTURE. YOU INFECT THEM WITH VIRUS. THEY MAKE NEW
VIRUS AT MAXIMAL RATE FOREVER AND ARE NOT KILLED. NO ANTIBODIES, NO
NOTHING TO PROTECT THEM FROM THE "DEADLY VIRUS". NOW THIS SAME NOT SO DEADLY VIRUS
IS PUT IN A HUMAN WHERE IT HARDLY REPLICATES AT ALL AND YET MANAGES TO KILL
MILLIONS OF CELLS, MOST OF WHICH IT HAS NOT EVEN INFECTED. THIS IS THE
SCENARIO OF HIV AND AIDS. DO YOU GET IT NOW?
Sorry for your flu. I hope your head clears soon.
P.S. I doubt very much that you have been productively infected by a rodent
virus, since in general there is quite an effective species barrier between humans and rodents, and if you did get so infected it would likely be catastrophic. You do maybe have antibodies to one or more rat viruses that might have recently tried, but no one would diagnose you as likely to come down with a rodent flu because of that or force rat
poisons into your system via a feeding tube. In fact you would be congratulated as being immune. Not so with HIV. Is this not even a
little paradoxical?
P.P.S. All of my epidemiological arguments refer to US HIV and AIDS statistics. Of course if you include Africa then the epidemic is growing, but that is after all the whole point of the great SA AIDS debates. Does AIDS in Africa even resemble AIDS in the US? How can a virus be reported by the CDC to be flat for 20 years in the US and by the WHO as increasing linearly from 1 per million to 25 per million in Africa over the same time without invoking fantastical and racially overtoned explanations mostly involving inconceivable amounts of promiscuous sexual activity? Etc
The answers to the questions regarding the levels of neutralizing antibodies and the inability of HIV to kill T4 cells in culture are related. Given that there are high levels of effectively neutralizing anti-HIV Ab in the blood of AIDS patients, and given that cells are not killed by HIV in culture, the inescapable conclusion is that the entire
immune system is required for HIV to do its dirty work, and that it does so by provoking an autoimmune response which would be independent of its replicative neutralization. It could certainly do this because of the omplementarity its gp120 protein has for the CD4 receptor. For example, an inappropriate, and unpredictable over time (hence also accounting for
the apparent paradox that disease does not follow infection in a predictable manner as with all other classical viral diseases), contact could 'induce' autoantibodies that recontact the CD4 cell in quite inappropriate ways that lead to cytolysis. A further virtue of this explanation is that it predicts the existence in symptomatic AIDS patients of exactly such autoantibodies. A quick PubMed search using "HIV, AIDS and autoantibodies" brings up a few papers that seem to offer
support for the ideas here, at least from their abstracts.
I would give such an answer an A, and reply as follows. Great idea, and you are correct in that there are a few papers presenting this
hypothesis and even offering some data in its favor. However, the data never held up and although "catalytic autoimmunity" remains the best scientific explanation of the basic HIV/AIDS virological paradoxes, it is finally an inadequate one.
P.S. The idea above was originally presented to me by George Poste in 1986, then the vice president for R&D at SmithKline, at a symposium in Singapore. The exact circumstances are described in the part of my book that immediately preceeds the back cover quote that recalls Tina Turner and Ronald Reagan in the same neural wash.
You infer pretty correctly sir as far as myself, Pres. Mbeki and a few other nutcases are concerned.
Actually of the respondents thus far, only two seem to fit your categorization.
IF this complete theoretical construction (see my book for the whole, sad and documented story of how this parlor room, back of the napkin supposition became NIH website fact) were true, HIV would cause AIDS. More to the point, it pretends to show a steep drop in neutralizing antibodies coincident with a decline in T cells and an increasing viremia. Why pretend that neutralizing antibodies are important if as caltechgal thinks "any first year grad. student" knows they are not?
Carry on. I just had to stick my nose in.
"As you know, the incidence of syphilis (a real sexually transmitted disease) continues to fall in South Africa. How then do HIV/AIDS believers explain the rise in HIV/AIDS cases? - they don't - silence is their answer. A fall in sexually transmitted diseases such as syphilis should be accompanied by a fall in HIV if HIV is sexually transmitted. The decline of syphylis in South Africa has nothing to do with treatment but is due to behaviour change. We are also beginning to see a drop in gonorrhoea and chlamydia cases."
(Yet HIV is of course said to be increasing by leaps and bounds.)
I am certain one of the Dean's World blogger believer-brains can come up with a self-delusional ratiocination of this paradox too.
Also by the way, most people in the U.S. seem to think that syphilus is a minor problem that can be easily fixed. But actually it's a quite horrible disease, really monstrous in its effects if it goes untreated for too long.
It's rather strange that some seem to think that we need the threat of AIDS to make people take safe sex practices seriously.
It is very late and you are obviously tired since you take my glowing praise of Cairo and my play with the word functional much, much much too literally and seriously. If relatively at peace and relatovely stable are criteria then indeed any number of African countries qualify: SA, Kenya, Botswanna, Senegal, Mali, Benin, Togo, Gabon for examples. Of these only SA has anything resembling a 21st C. independent economy and infrastructure, however. This is the reason of course that it is at the top of AIDS,Inc's list of disaster areas. It can AFFORD to keep the entire army in the war on AIDS -- an army that is increasingly finding it difficult to get the money to conduct operations in the US or Europe -- "combat ready 24/7", as I put it in Oncogenes, Aneuploidy and AIDS..."and even add a few special special forces".
When I wrote above: "you take my glowing praise of Cairo and my play with the word functional much, much much too literally and seriously." what I really meant was my glowing praise was real (I love Cairo) and you took my remarks too seriously as they were meant as playful.
When Dean wrote: "a rise in syphilis without a concurrent rise in AIDS would be very difficult to explain", I think he was simply endorsing Prof. Mhlongo's inference. If so, he might have less convolutedly written that a factual decline in syphilis incidence and a concurrent "said to be increasing" incidence of HIV infection are pretty damn incompatible...No wonder the AIDS establishment in SA doesn't have anything to say abt the "apparent success" of their safe sex campaigns!
I can only endorse 1000% Dean's last remarks about why do we find it necessary to tell people they will get a deadly, incurable disease if they don't use a condom when there are so many real and terrible STDs that we need to watch out for.
1] Siv causes aids in simians
2] Strains of hiv cause aids in simians
3] Kochs postulates are virtually fulfilled in regard to the hiv-aids model of causation.
The following is one argument why 3] is asserted. Basically it says that transmission of hiv to some people by others is clear, while noting 2] also:
"How HIV fulfills Koch’s postulates - http://www.hivnewsline.com/issues/Vol3Issue1/editorial.html
"The mainstay of Duesberg’s counter-theory is that HIV cannot be the etiologic agent in AIDS because it does not satisfy Koch’s famous postulates—postulates that must be fulfilled before it can be concluded that a particular bacterial agent causes a particular disease. Robert Koch, the discoverer of the anthrax bacillus, first posited his three postulates in the late nineteenth century (23), and although minor modifications have been suggested over the years—chiefly to accommodate technological advances (24, 25)—the basic tenets remain essentially unchanged. For more than a century Koch’s postulates have served as the litmus test for determining the cause of any epidemic disease:
1 - Epidemiological association: the suspected cause must be strongly associated with the disease
2 - Isolation: the suspected pathogen can be isolated—and propagated—outside the host
3 - Transmission pathogenesis: transfer of the suspected pathogen to an uninfected host, man or animal, produces the disease in that host
During the early years of the AIDS epidemic, both defenders and critics of the theory that HIV causes AIDS agreed that HIV failed to completely fulfill Koch’s postulates (1, 7, 13, 14, 25). As defenders of the theory were quick to point out, a number of other diseases, notably typhoid fever, diphtheria, and leprosy, also fail to meet these stringent tests of causality—yet there is no controversy about what causes these illnesses. We know the pathogens that produce these diseases; what we cannot do with consistency is culture those pathogens in vitro.
This was the problem with HIV as well, until recently. There was little question, even among the counter-theorists, that HIV clearly satisfied the first and second of Koch’s postulates, but it proved considerably harder to show that HIV also fulfilled the third. Today, however, overwhelming epidemiological and experimental data have been assembled to fulfill all three of Koch’s postulates, establishing to a virtual certainty that HIV causes AIDS (26).
Demonstrating the epidemiological concordance of HIV exposure and AIDS was relatively straightforward, once the etiologic agent had been identified. Numerous studies have shown, for example, that prompt and progressive depletion of CD4 lymphocytes—and a subsequent diagnosis of AIDS—follows HIV seroconversion in the vast majority of HIV-infected hemophiliacs (27, 28), and HIV antibodies have been detected in more than 90% of transfusion recipients who received blood from donors who were HIV-positive. In the latter group seroconversion has likewise led to progressive depletion of CD4 cells and the onset of AIDS (27-29).
Two recent prospective cohort studies of HIV-positive hemophiliacs have provided an even more direct link between HIV infection and mortality: They show a ten-fold increase in deaths among antibody-positive patients compared to uninfected individuals, irrespective of the severity of the subjects’ hemophilia (30, 31). Significantly, since the screening of donated blood for the presence of HIV was instituted, new infections have dropped almost to zero among hemophiliacs and transfusion recipients—further proof that HIV is the cause of AIDS.
The fact that HIV itself (or antibodies to the virus) can be detected in more than 95%—but less than 100%—of AIDS patients worldwide is explained by the relative insensitivity of the early tests for the presence of HIV in patients’ peripheral blood. By the more sensitive HIV RNA assays now used to detect the virus, it is possible to confirm the presence of HIV in individuals who have as few as 20 viral particles per mL of blood (see “The HIV RNA Assay: A Valuable New Diagnostic Tool,” Vol. 2, No. 2, pages 27-30).
Sensitive as these new diagnostic tests are, they will not detect HIV in all profoundly immunocompromised patients—not because the virus fails Koch’s test for pathogenicity but because other disorders cause the body’s immune system to collapse (32, 33). Certain drugs also produce immune suppression, as do chemical carcinogens, irradiation, and cigarette smoke.
The isolation component of Koch’s postulates has been repeatedly demonstrated since the discovery of HIV. Scores of isolates have been cultured from AIDS patients; the virus has been cultivated in fresh human T lymphocytes; and cultured-cell lines have been developed for in vitro propagation (10, 34). This leaves only Koch’s third postulate—transmission pathogenesis—as a matter of contention. Ethical considerations preclude the experimental inoculation of uninfected individuals with HIV, and this makes empirical verification of Koch’s last postulate exceedingly difficult.
Difficult, but not impossible. For while we cannot deliberately infect anyone with HIV merely to satisfy Koch’s postulates and Duesberg’s curiosity, we can examine the evidence that has been gathered on healthcare workers who were accidentally infected with HIV in the course of their professional work. Take, for example, the cases of three laboratory technicians who were inadvertently exposed to the HTLV-IIIb strain of HIV-1 while working with that strain in their laboratories (35). All three of these technicians developed antibodies to HIV, and within five years all three showed marked CD4 lymphocyte depletion. Two had their CD4 counts fall to less than 200 cells/mm3, and one of those developed PCP.
In all three of these cases it was possible to establish the precise phylogenetic type of the virus that had infected the laboratory workers. When genetic sequencing tests were performed on the laboratory virus and on viral samples taken from the three workers, the sequence divergence was less than 3% (36). This low level of divergence is equivalent to the variation observed in cases of HIV transmission from mothers to their infants—and it is less than one third as great as the extent of variation seen when viral samples from unconnected patients are compared (37, 38). Thus, these three unfortunate individuals provide prima facie evidence of transmission pathogenesis, Koch’s third postulate.
This same high level of genetic concordance was also seen when the C.D.C. compared viral samples taken from a Florida dentist who died of AIDS with samples taken from five of his patients who tested positive for HIV and who had no HIV risk factors other than multiple visits to the dentist for invasive procedures (39, 40). Two independent research groups reached the same conclusion after examining the HIV gene sequences of these six individuals: the dentist had almost certainly infected his patients in the course of those invasive procedures, although the experts could not say exactly how those infections had occurred (41-44).
It is unlikely that we will ever learn how transmission occurred in this unique cluster of infections, but the genetic data gathered from the victims of this tragedy teach us an important lesson: They establish, as conclusively as science can establish such things, that when HIV is inadvertently transferred from a person with AIDS to an uninfected host, it does indeed produce AIDS in that host (45). And thus it satisfies the last, and most rigorous, of Koch’s postulates.
Pathogenesis has also been demonstrated in various animal models. HIV-2, a less virulent strain of HIV largely restricted to West Africa, causes CD4 depletion and AIDS-like pathology in yellow baboons (46), and at least 12 strains of simian immunodeficiency virus, a close cousin of HIV, induce CD4 depletion and cause AIDS-defining illness in Asian macaques (47-51). Given that Koch’s third postulate can be fulfilled by transmission to either man or animal, these examples offer strong supplemental evidence that HIV causes AIDS."
Obviously your question was not directly answered, and it does seem odd that hiv has not been shown to cause aids in simians.
Thank You for your attention here at Dean's site!
I wondered when you would wade in with your copy and paste brand of scholarship. You get an F too. Didn't I write that simian AIDS was not relevant to an answer. Koch's postulates were not raised as an issue in these questions.I go through the logic of question 1 for you again: HIV researchers confidently infected chimpanzees with HIV since 1984 or so thinking that because the virus infects them so well (no species barrier problems) and since every other human pathogenic virus when infected into chimps causes an equivalent human disease, they were really quite surprised that until today no chimps get sick with AIDS or even AIDS-like diseases. Hence the reasons for the far fetched simian models (please read the paper I referenced to learn why these models are not like human AIDS in the least). The most reasonable explanation for this big anomaly is that HIV is NOT a human pathogen either.
Please do not quote anymore papers you copy from the web. I have probably read most of them and can assure you they do not contain answers that are acceptable either. However,you might have copied the references in the paper above as well since the citation numbers are meaningless without them (don't oblige me by doing that now).
I further urge you to read my sample answer and think about it for a while. If you would like to comment on that, I will probably answer you.
I wish I could thank you for your attention.
Easy. Poor correlation between AIDS (however you choose to define it) and HIV infection.
Basically, large percentages of HIV- patients with AIDS.
Prof. Bialy apparently will not accept answers which are not "referenced", i.e. demonstrated experimentally.
So what's wrong with people not believing him until he experimentally demonstrates that HIV does not cause AIDS, instead of pointing to holes in other people's theories? This isn't just a hypothetical question. It's what the AIDS community has been doing.
In other words, The AIDS community thinks that not having definite answers to Bialy's questions does not disprove their hypothesis. How am I to know that they are wrong?
"I wondered when you would wade in with your copy and paste brand of scholarship. You get an F too. Didn't I write that simian AIDS was not relevant to an answer. Koch's postulates were also not directly raised as an issue in this question, although it does involve the most important of these logical imperatives. (My book has an extensive, and if I do say so myself, excellent treatment of the postulates of Koch and Henle and Duesberg's arguments over the years that involve them). I go through the logic of question 1 for you again: HIV researchers confidently infected chimpanzees with HIV since 1984 or so thinking that because the virus infects them so well (no species barrier problems) and since every other human pathogenic virus when injected into chimps causes an equivalent human disease, the chimps would get sick. They were really quite surprised that until today no chimps have come down with AIDS or even AIDS-like diseases — hence the reasons for the far fetched simian models (please read the paper I referenced to learn why these models are not like human AIDS in the least). The most reasonable explanation for this big anomaly is that HIV is NOT a human pathogen either
Go to duesberg.com and download a paper there entitled "The Gap in HIV/AIDS Reporting" (or something very close to that. I cannot take the time now to quote it exactly for you but it is easily found on the website)that was published in Bio/Technology in 1990 or thereabouts. It will provide you a complete accounting that will answer your desire expressed above.
...they were really quite surprised that until today no chimps get sick with AIDS or even AIDS-like diseases...
This implies to me that someone very recently has managed to get a chimp sick this way. I assume this was not your intent?
(Well hey you caught me fumbling my words too... heh.)
The period since then is much more troubling since the symptom list for AIDS exploded in the early '90s.
It's nice that he points out that overreporting may have caused the appearance of a strong correlation between HIV and AIDS, but I would prefer actual studies showing no strong correlation, preferrably recent ones using the best diagnostic technology.
Maor: As we have discussed so many times, the current diagnostic standards from AIDS are wildly different from what they were in the 1980s. They are hugely broad. From everything I've seen and read, the HIV research community refuses to give a definition that can be rigorously defined. So what you're requesting is like trying to nail Jell-O to a wall.
Find for me in the literature for today (because we cannot go back in time) what the exact definition of AIDS is. Monomer couldn't do it--he was merely convinced that somehow, in some way, a non-slippery, non-tautological definition of AIDS exists somewhere. You appear to be under the same impression.
If so, where is it? What is it? Without it, the study you want done cannot be done.
This is exactly what Miklos was complaining about in the letter I published from him, by the way.
If he cracks you up, you should see what he wrote on my site,smacked me down pretty good for off handedly comparing this HIV=AIDS debate to the gun control debate.
Lesson learned, do not compare a scientific debate to a political one.
Thanks again Dr. Bialy.^_^
I've said specifically that it doesn't matter. Any symptom that strongly correlates with HIV should be suspected of being caused by HIV. Any symptom which doesn't, apparently isn't caused by HIV. If there are no serious symptoms caused by HIV, then HIV doesn't do anything bad. If HIV does bad stuff, we'll call the bad stuff AIDS. Each symptom can be looked at seperately.
If you can only do one study, I recommend T-cell depletion as a good thing to look at, because it is claimed to cause the other problems. While there may be confusion about some symptoms, no one will say that T-cell depletion is not a symptom of AIDS.
I am truly delighted that you each find me an amusing fellow. Oncogenes, Aneuploidy and AIDS is pretty damn funny in places too. The overall story is more like a Greek tragedy, however.
Odabo,
Dr. Tryptophan - a name bestowed upon me by my Nigerian students , who were very clever punners in the English as well as Yoruba languages, in 1976 when I was a lecturer at the University of Ife in Ile-Ife, Nigeria.
----------------
Dean - Until today no chimps have gotten sick with AIDS. Maybe tomorrow one of them will catch cold and it will make the cover of Nature.
Monomer - Do you know what a tautology is? How bout an oxymoron? Perhaps unique in the worlds of grammar and virology, the standard definition of AIDS is both. Why do I have the distinct feeling that you will always prefer something that reinforces your evidently difficult to arrive at opinion to a good knock in the noggin. Scientists, by the way, ALWAYS prefer to be knocked on the noggin. Please read the first chapter at least of my book. You can do so in your favorite form ...online. It is all about the construction of the molecular biologist's head in molecular biology's intellectual salad days of the 60s.
Maor - Do you know what a tautology is? How bout an oxymoron? Perhaps unique in the worlds of grammar and virology, the standard definition of AIDS is both. Why do I have the distinct feeling that you will always prefer something that reinforces your evidently difficult to arrive at opinion to a good knock in the noggin. Scientists, by the way, ALWAYS prefer to be knocked on the noggin. Please read the first chapter at least of my book. You can do so in your favorite form ...online. It is all about the construction of the molecular biologist's head in molecular biology's intellectual salad days of the 60s.
In defense of the "average smart person's" perspective, this is all rather akin to being told that George W. Bush won the elections because his alien masters from the planet Klaatu arranged things for him, furthermore, John Kerry is actually a member of George W. Bush's inner circle and secretly contrived to lose the election.
Flatly impossible? No. But if people look at you and say, "Uhm.... What?" this should not be entirely surprising.
The problem here as I see it is that the proof for the extraordinary claim--that everything you thought you knew was wrong--requires slowly unravelling a large number of assumptions. The skeptic should not be blamed for his skepticism. His tools are limited, and while he may be smart he is not equipped to slap down every claim.
If you think my allusions to aliens and whatnot above is entirely off-base, I must tell you I have a member of my family who believes things not too far at all removed from what I just described about the elections.
Furthermore, if he is proven wrong he may well feel like a complete fool, which is hard for anybody to go through.
Although there's a trick to that--if you embrace being wrong about something, it's liberating.
I believe Dr. Bialy has presented more than enough to make people say, "Hmmm. You've seriously made me think about some things." Now... do you have the energy to say, "all right, I want to learn more?"
Note that I do not say (and have never said) that HIV does not cause AIDS. I have said repeatedly that I have an awfully strong suspicion here, that things simply are not kosher here. I've known most of what Duesberg, Bialy, et. al. have mentioned for some time now. I honestly believe that Wince &Nod's statement above describes my exact position better than anyone else's.
"These people are on to something, and ought to be taken seriously becuase they are not fools" strikes me as a fairly sane response.
I have something tangentially related to this that I think I will post today.
I cannot account for your feelings.
I'm a bit busy to start reading books just now, especially when the relevance of the subject is unclear to me.
I know quite a few scientists, and I'm fairly familiar with their thinking.
I have told Dean already why I don't consider tautological diagnoses illegitimate. It seems to me that doctors frequently use this logic:
-Patient has certain symptoms
-Patient has contagion X
-Contagion X is thought to cause these symptoms
-Therefore, patient apparently has a disease caused by contagion X
Now, how is AIDS different?
You are making a gigantic sandcastle in the ionosphere when you describe a hard-nosed spouter of an orthodoxy as a skeptic. The use of this term in relation to the previous would more properly be "a skeptic of the skeptic's position".
As far as our friend, Dr. Maor, MD (I am guessing)is concerned when he demands that HIV sketics disprove the hypothesis, he is creating something much less substantial than even your sandcastles in defense of a blogobuddy. Read my book and learn with great clarity and even a chuckle or two the following: The HIV hypothesis has never been falsifiable, by anyone. Therefore it was never a scientific hypothesis to begin with. We in the insurgency continue to refer to it that way for the express purpose of calling attention to this important fact, and to remind people that the essence of experimental science is the design and testing of FALSIFIABLE hypotheses and that AIDS science has never been that. HIV equals AIDS sprang full blown and untouchable from the brow of the NIH in a grotesque mockery of Athena springing from the brow of Zeus. Since that time there has been concerted and effective effort to suppress all attempts at falsification such as pretending the six (million) contradictions between HIV/AIDS virology, epidemiology, biochemistry, genetics and medicine and traditional versions of these disciplines do not exist or are unimportant because millions in Africa are being infected by overpaid, sexually maniacal truckers every ten minutes, and villages are disappearing overnight as though hit by a biological tsunami.
Mmmmmmmmmmmmm. Dr. Maor sounds so nice :)
I'm not trying to get you to believe the HIV hypothesis.
I think it's overreach to say that the questions posed are "fatal" to the HIV hypothesis.
I'm suggesting that there's evidence supporting the HIV hypothesis, evidence contradicting it, and some people can say that the "pros" outweigh the "antis" enough to consider the hypothesis proven, while others can believe the opposite and NO ONE IS DOING ANYTHING WRONG, BECAUSE "PROOF" IS SUBJECTIVE.
I think that demonstrating a lack of correlation between HIV and any symptom associated with AIDS would falsify the association between the symptom and HIV. Falsify the association for all the symptoms and you falsify the HIV hypothesis. What's so hard about that?
That works in both directions.
I think it is legitimate for different people to consider the HIV hypothesis as "proven" and "disproven".
If the former greatly outnumber the latter, and thus end up being responsible for summarizing things for the public and handing out taxpayers' money, it's not necessarily unkosher for them to ignore the minority. Because they sincerely consider their viewpoint to be proven, and they have an important job to do.
Of course, rudeness is just plain wrong.
Science is not consensus. Consensus is not science.
As soon as a scientist starts counting the heads of his collegues, he is no longer a scientist.
Shortly after leaving Germany, Einstein was informed that hundreds of German physicists had signed a petition stating that his theory of relativity was "dubious and Jewish science".
The great man's answer:
Why so many? It only takes one if you have proof.
NOBODY POST THEIR FAVORITE EINSTEIN STORY
I respectfully disagree with your response, and that's how science works. I agree that there's no quick answer, and I wouldn't presume to say that what I put forward are the answers, just points for consideration and caveats to your arguments, but obviously you didn't consider that, or maybe I wasn't clear on that. It's also clear that you think that some of my points are beneath consideration without bothering to explain why. I never claimed to be an expert in this field, merely interested in why the HIV/AIDS relationship has to be all or nothing.
I still stand by my argument that the in vitro experimental results are less valid than in vivo observations. But by the same token, it doesn't invalidate the results of in vitro experiments. Nor does it lessen the impact of in vitro results as compared to other in vitro results. Rather it provides a basis for understanding the differences in mechanism between dish and body.
As for this statement:
That's actually out of context, no specific experiment, least of all neutralizing antibodies was the object of that comment, in vitro results in general were. (for those less familiar) In the case of antibodies, looking at antibody levels from blood/tissue samples is considered an in vivo experiment, while looking at antibodies produced by cells subsequently cultured from the same sample would be considered an in vitro experiment.
I think it's highly presumptuous of you to just "grade" my response when the object here is a discussion rather than a class. Rather than simply pointing out the logical fallacies in my argument and set down what you feel is the more accurate point of view, you had to begin with some ad hominem (if academic) garbage. If I wanted a grade, Dr. Bialy, I assure you I would become familiar enough with field to present a complete and coherent argument in favor of my hypothesis and I would get an A, just maybe not from you, since our conclusions on the subject differ.
I hope that my objection to your response is not taken improperly. I think that would be counterproductive since we agree on some points. Like you, I wonder about the motives behind the total acceptance of the HIV-> AIDS hypothesis and the validity of the current model based on the data available, but we disagree on the extent to which we are willing to give creedence to the current model.
#1 Sure, chimps get infected with HIV, but they show no symptoms. My point was that this is not the only example of infection without productive infection. So what if this is the ONLY virus without a productive infection? Science is based on what we learn from "exceptions to the rules". Humans carry a number of antibodies to "animal" viruses, which indicates infection, if not a productive or symptomatic infection. One of these viruses is SIV. My point is that if humans carry SIV antibodies and are asymptomatic, why is it such a leap to see chimpanzees that express HIV antibodies that are asymptomatic? Stating that SIV is irrelevant is a logical fault because that presumes that viral infection can only go down the evolutionary ladder instead of both ways as we see in a number of other diseases. I don't understand how you can make the claim that it is telling that a human virus is asymptomatic in chimps without even considering what it means that a primate virus is asymptomatic in humans. Answer that, or clarify your question.
#2 I realize that I was making a rather simplistic argument about the ab problem, and I acknowledge that you are right. However, I don't understand how you can argue that PCP prevalence is a purely statistical measure. What is your basis for this declaration? Here's an analogy to explain my point: If the world is uniformly covered with a layer of dirt (normal dirt, whatever type you like), and everyone rolls in it, only the people who are wet already are going to get muddy, and the rest will cover a spectrum from dirty to dusty to clean, depending on how they roll around. In this analogy, PCP is the dirt.
More to come.
please caltechgirl...basta. i will not answer questions from you or further attempt to educate you in basic virology/immunology/genetics and epidemiology. the point of my 6 questions has been made very clear numerous times in this scroll...it was to get you to think about a lot of data that makes your favorite hypothesis less than the favorite of classically minded molecular bilogists like myself, Duesberg, Gilbert, Mullis etc. it was expressly not for the purpose of getting into specialist arguments on a clearly nonspecialist website. i thought i did a good job of marking your original essay with a minimum of ad hominem remarks and a lot of information. the logic of in vitro and in vivo and the chimp experiments still elude you. keeping your door is as you know the wrong overall strategy.
good luck. you need it.
tryptophan
Farr's law aside, the way I have thought of this is like receptor pharmacology, which is probably too complicated to put forward in this format, but to sum up, for any given population of receptors, there are maximal number of bindings (and thus electrical transmissions) for any given length of time, based on the number of receptors and the number of molcules of transmitter available (opportunities for binding). With AIDS, it seems as if there is a maximal number of transmissions in a given population, based on the number of patients and the number of opportunities each has to transmit. This is a static number in pharmacology for any given length of time (Bmax, I think, but I'm no pharmacologist, so I'm not sure which constant it is exactly), but it can be affected by drugs or genetics, and change to adifferent static number(eg. Bmax'). Similarly, perhaps, the number of AIDS transmissions is being held to a Bmax' based on behavior, drug therapies, and perhaps even background genetics. Although I suspect you disagree with the data, there are published reports that drug therapies decrease transmission. If this interaction is the case, then what phase of the epidemic we stand in remains unclear.
And BTW, Harve, for future reference, nodody refers to a colleague or a peer as "dear" in a scientific conversation.
I have tried to discourse with you with nothing but respect, as I would any colleague, and I was honestly trying to have a real conversation with you based on what I understand and what you believe, and to try to understand what you disagree with, but all you seem to be interested in is patronizing me an denigrating me because I disagree with you. Too bad. Maybe we both could have learned something here. Obviously you don't feel like you need to.
i was just abt to type this anticipating exactly such a response from you.
dean has my phone number. if you are really interested in having a serious discussion about data and not beliefs, i will be more than glad to speak with you as a colleague for as long as you wish. i only have no interest in pursuing this discussion in the blogosphere where one is obviously writing with an audience in mind and this affects the quality of the discourse.
Science does work like that frequently. Maybe that's not a good thing. It's not my fault, though.
If proof is not subjective, fine, then there is little or no proof in science. I don't mind.
"A Hypothesis must make predictions that are testable in an objective manner that will either falsify the hypothesis or not."
Prediction: Certain symptoms will always be correlated with HIV infection, because HIV is thought to cause them.
This has been the case so far. Several symptoms are far more common in HIV+ people than in HIV- people. If this had not been the case, the HIV hypothesis would not be so popular today.
Now, this doesn't PROVE anything. So a prediction was fulfilled. Ho hum. That's not logical proof. Correlation does not equal causation etc. Would you believe every idea that produced a successful prediction? I sure wouldn't. But it does make it more likely that the theory is true. How likely? That's SUBJECTIVE.
Other theories are the same way. Take the laws of thermodynamics. They always seem to hold. So? Does that PROVE that they ALWAYS do? I don't think so. So why are physicists usually so confident about them? Even more than other theories which have never been seen to be violated? Part of it has to do with the fact that they SEEM right. They feel true. Purely subjective. The fact that the laws have never been seen to be violated supports them to a great extent. But PROOF? Nah.
"if HIV causes AIDS, when the HIV virus in introduced into chimps, it will cause AIDS symptoms in at least some of the chimps."
Not everybody would predict that with confidence. AIDS is a human disease and while it may seem PROBABLE, even HIGHLY PROBABLE, that chimps would get a human disease, how probable are we talking about? That's subjective.
"Science is not consensus. Consensus is not science."
I never said otherwise. I DO think that nothing in science is "proven" logically, at least not in biology. What happens with successful theories is that the probability that it is true grows until it is high enough to be considered "true". When does that happen? It's subjective. So there's nothing wrong with someone considering a theory true, when others completely disagree. Because objective proof will never happen.
1] I'm not going to read Duesberg's paper alleged to disprove the relevance of the Chimp model. Some specialists are apparently not convinced by Duesberg, and the Simian findings so far are still suspicious, although it is your right to declare them irrelevant if you want to. [Nor does the fact that the Journal of P and T has a rigorous review process constitute anything like an absolute endorsement of Duesberg's paper in particular.]
2] The Koch's Postulates evidence still seems at least suspicious regarding this whole issue. I'm not going to read your book on it because I don't want to, for various reasons. I'm simply going to assume that a lot of specialists in infectious disease know what Koch's Postulates are.
3] I don't know what my allegedly characteristic copy and paste tactic has to do with it, unless your are worried someone might read what is pasted.
Thank you for the effort you are putting into this discussion.
enuf spleenful if instructive preamble.
now, dig - as my man miles would have sd it:
there is a significant difference between two groups of scientists setting out to test dueling hypotheses, and two groups of scientists in which one group is honestly trying to experimentally test an experimental hypothesis and another that is 100% convinced that its hypothesis is correct and therefore any and all experimental data that the other group produces, either from their own laboratories or from accurate and honest citation of contradictions in their own published data, are simply relegated to realms of 'there is obviously some other explanation and eventually we will figure it out if you give us enough money', or the results are dismissed with the kind of out of hand and off the cuff remarks that have issued from the keyboards of some contributors to this (and as far as I can tell most every) dw discussion thread. i may have just written the longest sentence of my life, but it is comprehensible.
remember guys and gals: if your only tool is a hammer, every problem looks like a nail.
The syphilis rates in Africa could be left in the dust by hiv-aids rates if syphilis was not screened for at the same rate as hiv. I don't know if this is the case, but screening tests for hiv are more simple than those for syphilis.
And, briefly, the failure of pneumocystis to be the predominate aids disease can possibly be due to prophylaxis based on CD4 counts. "Ubiquitousness" is not the force it might seem to be. Candida is also ubiquitous, prophylaxis has different efficacies for different diseases, etc.. The CDC does not even mind if patients with hiv positivity and decreased CD4 counts are held in the same room with people who have PCP, so long as they are prophylaxed for PCP:
"1. Although some authorities recommend that persons with human immunodeficiency virus (HIV) infection who are at risk for P. carinii pneumonia (PCP) not share a hospital room with a patient who has PCP, data are insufficient to support this recommendation as standard practice (CIII)." from the CDC site
Maybe my thoughts are not totally thought out, but they are more than I've related here and seem possibly explanatory to me so far.
The Koch's postulate argument and the efficacy of treatment argument look difficult to overcome.
but foist: the 'comprehensible' overly long sentence above should really be ammended — my realest, no tongue in any cheek at all apology to you all for this really inexcusable lapse in rereading something i typed as fast as i could —- minimally,as follows:
"there is a significant difference between two groups of scientists setting out to test dueling hypotheses, and two groups of scientists in which one group is honestly trying to experimentally test an experimental hypothesis and another that is 100% convinced that its hypothesis is correct and therefore any and all experimental data that the other group produces, either from their own laboratories or from accurate and honest citation of contradictions in the published data of the others, are simply relegated to realms of 'there is obviously some other explanation and eventually we will figure it out if you give us enough money', or the results are dismissed with the kind of out of hand and off the cuff remarks that have issued from the keyboards of some contributors to this (and as far as I can tell most every) dw discussion thread. i may have just written the longest sentence of my life, but it is comprehensible.
making that syntactical correction was not, however, what prompted more "fumigation of my wisdom on this court" as richard pryor once hilariously put it in a film, from this abrogado for occam and his for real, deadly razor.
no, what prompted this, which most of you have already ceased to read, furtherance was in fact my neurotic, some would say, passion stated way now above.
so here i go with another attempt to make the same basic point:
we go back to the chimps....as caltechgal rightly pointed out our closest genetic relatives (they differ from us lower primates in that although they have esssentially the same genetic repetoire as us...only a few thousand at most individual genetic differences, which are much to small to account for the gigantic differences between ourselves and these clearly superior beings (not all joke here at all . and on the point abt too few gene differences to account for cheetah and bozo the president it is 100% serious.. check the specialist literature...there is no disagreement on this point). so what's the reason we are so different? we have 46 chromosomes and 35000 different genes, they have 47 chromosomes and the same 35000 genes. this directly leads into a discussion of aneuploidy and cancer but it is for another time, even if perhaps the same place.)
boy do i digress.
now we go back to the elucidation that began "we go back to the chimps":
the freely admitted inability of hiv to cause aids or even aids-like diseases in productively infected chimpanzees after so many have been infected for so long as shown by their highly active hiv ab tests, and have never, ever been given an experimental, or even approved aids drug (it was tried once but the humane society prevented it...not so the harlem children trials all readers of this know abt)is soooooooooooo devastating to the hiv/aids hypothesis that the onliest solution that the geniuses of hiv/aids could come with to this completely clear experimental failure of koch's third postulate in the very, very, very, very, best imaginable nonhuman host, and one that had never, ever, ever, ever failed them before, was to concoct a totally non-aids like animal primate model in african green monkeys (further from chimps than chimps are from us by far and way)and continue despite all attempts to show point for point why the animal models are so bad (maor above is typical...i won't even bother to read it. believe me i have heard that one from a lot bigger names than ma(j)or), they continue to insist that these models prove koch's third postulate because something utterly mysterious is going on with chimps and hiv. something so mysterious they will not even try to understand it but simply handwave and handwave knowing that it doesn't matter in the least what the data are or what the nutcases say because any tear in the comforting linus blanket with which hiv has been so expensively and carefully wrapped, will be magically healed.
What precisely did you advise President Thabo Mbeki regarding the proliferation and prevention of HIV/AIDS in South Africa ?
send me an email address through dean and i will send you a copy of the report of the panel. it perhaps can still be downloaded from the sa gov website, but i haven't checked in a while so i'm not sure.
alternatively dean might have a simple way to make the document available to everyone.
or alternatively you could read chapter 5 of my book online page by page on amazon if you do not want to invest in purchasing a copy.
some might call me a pedant...even me but i want to make a completely non-pedantic point by the analysis below. the point is that if you cannot think straight enuf to write accurate english, how in the world can you presume to have the neuronic horsepower to go through a scientific argument in which each word has a very specialized and definite meaning (how could it be otherwise and be science and not semantic word play, which is what some of you think is the same thing)our language and our thinking are inextricably bound like the two strands of the golden helix. onvious and perhaps trite, but not because of that any less true.
here is my demonstration, interlaced in CAPS: you wrote above
"I'm not going to read Duesberg's paper alleged to disprove the relevance of the Chimp model. Some OTHER? SPECIALISTS OR DOESN'T THE PERPETRATOR OF THE ALLEGATIONS QUALIFY?specialists are apparently not convinced by Duesberg, AND THIS IS A REASON IN YOUR VIEW TO COMPLETELY IGNORE 75 PAGES OF INTENSELY PEER REVIEWED WRITING? and the Simian findings so far are still suspicious,WELL MONOMERIC ONE IF THE SIMIAN FINDINGS ARE SUSPICIOUS (OF WHAT ARE THE SUSPICOUS OF MIGHT I ASK)THEN WHY DO YOU TAKE THEM SO SERIOUSLY. OBVIOUSLY YOU MEANT THAT YOU HAD SUSPICIONS THE SIMIAN FINDINGS MIGHT BE IMPORTANT although it is your right RIGHTS I ALWAYS THOUGHT BELONGED IN THE REALM OF THE POLIS to declare them irrelevant if you want to. [Nor does the fact that the Journal of P and T has a rigorous review process constitute anything like an absolute endorsement of Duesberg's paper in particular." IT IS A CLEAR ENDORSEMENT WHEN A JOURNAL PUBLISHES A PAPER THAT THE EDITORIAL BOARD OF THE JOURNAL HAS PUT ITS STAMP OF APPROVAL ON THE FACT THAT THE PAPER IS CAREFULLY COMPOSED AND THAT ITS LOGIC AND CONTENTIONS ARE DEFENSIBLE BY THE HIGHEST SCIENTIFIC STANDARDS THAT THE BOARD AND ITS BOARD OF REVIEWING EDITORS CAN MANAGE. DOESN'T THAT SOUND PRETTY ABSOLUTE? MAYBE YOU CANNOT CONSIDER ME AN HIV/AIDS SPECIALIST, BUT I HAVE A HARD WON REPUTATION, EVEN AMONG MANY OF MY SCIENTIC AIDS ADVERSARIES, AS BEING NOTHING IF NOT A COMPLETELY PROFESSIONAL SCIENTIFIC EDITOR.
to all my new dw friends and foes
tonight at midnight cst will be the last possible time i will post anything to this discussion
some (which means at least one, possibly all remember) will cheer. one or two might have a quickly passing vague regret. nonetheless it need be so.
i do, if you can believe it, have one or two other things to which i need to turn my febrile attention, and i really cannot imagine that any more of my "fumigations" here can make any further difference of even the slightest import. (like the difference between 2000 and 2001 degrees of temperature, as a favorite berkeley prof was fond of saying to classmates who insisted on occupying the microbalances in vain attempts to weigh exactly 0.1346 mgs of some chemical to make a solution of o so precise molarity that was intended for use as a dialysis buffer. to not give the wrong impression of prof. pigpen as he liked to be called, he also said much more often to me the even better and more useful adage: how come there is never time to do it right, but always time to do it over?.)
either i have written enuf here (or as some will say...too much)to entice a few to pick up a book that took me four years to compose, or i have provoked at least a few to think a bit differently than they previously thought concerning the epsitemological and etiological bases of the "hiv/aids" pandemic. whether either, both or neither, i have enjoyed myself more than i can say and i thank you all, blog friend and foe alike for making this possible.
but be also fairly warned,
like the hollywood sequel, or the spanish inquisition, i could be back when you least expect me.
harvey
You are clearly, the biggest asshole that has showed up here on DW. But that is only one opinion.
Mandela announces eldest son died of AIDS
Former President Nelson Mandela announced Thursday that his eldest son died Thursday of AIDS-related complications, saying the only way to fight the disease's stigma was to speak openly about it.
Makgatho Mandela, an attorney, was admitted to Linksfield Park Clinic last month. He died at age 54.
"Let us give publicity to HIV/AIDS and not hide it, because the only way of making it appear to be a normal illness, just like TB, like cancer, is always to come out and say somebody has died because of HIV," Mandela said at a news conference at his residence.
Mandela's position contrasts with that of President Thabo Mbeki, who has denied knowing anyone who died of AIDS. Mandela declined to comment on Mbeki's views.
More than 5 million of South Africa's 45 million people are infected with HIV, the virus that causes AIDS, more than in any other country. An estimated 600 die of AIDS-related complications every day.
Dr. Bialy, above, you say: "the freely admitted inability of hiv to cause aids or even aids-like diseases in productively infected chimpanzees after so many have been infected for so long as shown by their highly active hiv ab tests". But the NIAID Fact Sheet at the NIH site says: "Chimpanzees experimentally infected with HIV have developed severe immunosuppression and AIDS." They list several references in this section, so I don't know which connects to this specific assertion, but here is the link.
On that same site, they also state that 25 of 56 health care workers who were accidentally infected developed AIDS in the absence of any other risk factors.
My apologies if these have already been addressed. I'm just trying to understand a debate that, before yesterday, I did not even know was happening. Thank you, Dean, for bringing it to my attention, and thank you, Dr. Bialy for your contributions.
darn. you spoiled my dramatic exit, thanks to catchem 22, because this is a question that i cannot avoid answering. anyway, i still have another hour before my self declared m