https://web.archive.org/web/20040804020325/http://www.sumeria.net/aids/chat.html
Dr. Stefan Lanka answers critic Steven B. Harris M.D.'s rejoinder to his paper, "HIV: Reality or Artefact".
Dr. Steven B. Harris will no doubt consider it an impertinence even to respond to his "rebuttal" of the thesis I put forward in my article on HIV in the capacity of a "purported" virologist, striking as it does at the very bedrock of his credo. I console myself that while I make no claims to infallibility, I have no doubt that I am a virologist, moreover, one motivated only by altruism, and untroubled by any worries that I may have dispatched any friend or patient to an entirely unnecessary and painful death, through craven obeisance to an ill-thought out medical theory concocted by a French mediocrity who, right from the start, doubted the validity of a virus-only theory of AIDS causation and only last week unleashed a new wave of doubt; and an American scientific gangster who had committed so many crass, self-aggrandising blunders in the previous decade, that he could not really be relied upon to tell the time correctly.
I have also not forgotten the First Commandment of my profession: above all, do no harm!
It is, of course, only supposition on my part to think that elementary cell biology forms any part of the curriculum of medical training of American doctors. If so, it is astonishing that Harris has either forgotten it all, or is wilfully ignoring it, for reasons best known to himself.
That said, I must compliment my critic on his courage and relative erudition, for it is not often that, in my admittedly still limited experience of life, a mere doctor knowingly crosses swords with a molecular biologist/virologist on the latter's home ground. Doctors are normally more at ease speculating about the vagaries of epidemiology than engaging in disputation with the practitioner of an exact science.
Harris's simple mistake is to have ignored well-known intracellular structural particles common to all metabolically active cells, of which there are many - specifically, what are called "coated vesicles". Their function is to transport metabolic decay products out of living cells.
This is hardly a pardonable error, since basic prudence on his part should have led him to study fairly closely the differences between electron micrographs of microsomes in general, and coated vesicles in particular, with or without the help of a specialist in this field - it did after all form one of the two main planks of my article. Neither virus particles nor cellular particles are rarities in the literature. Contrary to Harris's little joke, I have spent an enormous amount of time in libraries, far too much of it wasted trying to make sense of the mile upon mile of bookshelf devoted to the riddle of "cancer-causing" viruses (of which more below). Harris clearly would have benefitted hugely looking down an electron microscope more often, and allowing himself to be enchanted by the multiplicity of such "Harris" viruses, more widely known as coated vesicles. This would have made him realise that their very ubiquity in healthy tissues meant they could not be responsible for any pathogenicity.
Harris's strategy appears to be to launch a shut-out bid by declaring HIV to be a lentivirus, as if that explained anything. Lentiviruses are an even worse case of virological muddle than HIV, in that they, too, have never been isolated nor proven to do what is alleged of them. Fiddling around with them has been going on for 20 years at least - to no effect - whereas with HIV it has only been 10! One very important difference, though, between the two situations is that lentiviruses have at worst affected only a handful of animals with so little consequence, that most scientists would be hard pressed to say anything about them, whereas HIV has spawned one of the worst mistakes in the annals of medicine, a veritable nightmare for those affected, and a significant impairment of the quality of life of those who just live in Dread of it.
Whether lentivirus or not, it is a nullity ab initio to seek to prove anything in science by arguing by analogy. That is the negation of the scientific method. Whatever may be true of FLeV, FIV, SIV etc. has no bearing on the existence or function of HIV. Points of visual similarity do not constitute proof of identity nor function. To assert otherwise means either that he has never looked properly at electron micrographs, or he is deluding himself.
The fatuity of his reasoning is highlighted (quite fortuitously) by the recent "discovery" that HIV is most definitely not a lentivirus. Lenti- means slow. Because since January 1995, don't we have it on the highest authority that HIV replicates very rapidly, at a rate of 1000 million particles a day, every day, for an average of 10 years? Anybody with an ounce of common sense must have realised that a virus cannot have been barely detectable for the first 10 years of its existence, then suddenly turn out to be "hyperactive" after all. The answer to this conundrum is quite simple: AIDS science is not science at all, just empty posturing as such. Proper science is never made at press conferences, it does not operate by decree, it is not a matter of developing a consensus, and it should not totter from "revelation" to "revelation", with theory made "on the hoof", a hodge-podge of mysterious mechanisms requiring further billions to finance an army of scientific bureaucrats.
Inexplicable failures in the predictions of a scientific theory should spell its death. That is the essence of the scientific method. Consistent failure in respect of HIV should long ago have sufficed to dismiss it as a cause of AIDS. That it continues nonetheless, makes it just an article of faith, and reduces belief in it to the status of a religion.
An analysis of Dr. Steven B. Harris's answer to my paper "HIV: Reality or Artefact" has just appeared in Continuum Magazine (London), June/July 1995 (tel +181 961 1170, fax +181 961 2330).
The format adopted there was of stating the point at issue followed by Harris's comment with my answer to that, juxtaposed. To pursue this format here would clearly become very unwieldy, and the use of photographs on e-mail transcends my technical expertise. I have, therefore, summarised the points raised by Harris, and appended my answers to them.
Dr. Harris is clearly quite an intelligent man, so his very first point "Strangely enough, Lanka does not explain what we're seeing in all those electron micrographs" has me tearing my hair out, because a few paragraphs further down he provides his own answer that "less well-known is the existence of other particles which look like viruses but aren't, and are nonchalantly referred to as "virus-like" particles. Such particles are far from rare, found, for example, always in placentas, and very frequently in the artificial environment of laboratory cell cultures. They have served to muddy the waters considerably as far as AIDS research is concerned, because particles just like these have been called HIV."
What is one to make of such crassness? Is the whole AIDS tragedy currently being played out just a little game for Harris? It is a property of all biologically active cells that they contain intra-cellular particles called microsomes, perixomes and lysosomes, which are particulate in nature, and to the untutored eye could be mistaken for virus particles. Harris seems to forget that most people can actually think, and flip back to see what has been said before, a number of other such howlers (deliberate deceptions?) will be pointed out below.
Harris then describes some properties of lentiviruses, which are an entirely separate issue. It is true that while these have a recognisable shape (as opposed to being just an amorphous mess), and do indeed have what appear to be knobs (the famous CD4 receptors) which shear off so easily, this to a proper scientist does not suffice to make them viruses. Sorry! Microsomes, perixomes and lysosomes also have recognisable shapes and many have spikes of some kind on them. The important point Harris cannot or will not comprehend is that these lentiviral micrographs are never of the viruses he is so fond of quoting, but are always interspersed with other structures and debris, which is crucial to my case.
Harris goes on:
"HIV-1 and HIV-2, the two viruses isolated from human AIDS patients..."
If they had indeed been isolated, as he claims, nothing further need be said; the whole point is that they have not been isolated, indeed, the title "isolated viruses" occurs several times in my references which does not mean they have actually been isolated, of course.
Harris's attitude is quite extraordinary. He admits that "there are existent studies in which less than perfect-looking particles have been called HIV, and assumed to be HIV, but some of these studies have no doubt also seen cellular debris or other retrovirus which can be mistaken for HIV or other lentiviruses if not all identifying features are present. However, there are quite enough studies in which all the lentivirus characteristics noted above ARE present in EM photographs, and morphology is considerably more clear. In these studies, the viruses in the electron micrographs are clearly either EIAV, FIV, SIV, or HIV-1, or HIV-2."
Yet the caption to the micrograph Harris quotes repeatedly, clearly states "sections of co-sedimented HIV and latex spheres ... along with membranous and macromolecular debris ..." Out of his own mouth therefore he admits that these isolated particles are not true isolated particles, but a heterogeneous mixture containing unspecified impurities. What is the matter with the man! In case anybody is wondering why there are latex spheres present in Harris's virus isolation: well, they are there to stop the particles from crushing each other. In other words, if they were not there all the "HIV" particles would disintegrate. The use of latex condoms may therefore be contra-indicated, because they may inadvertently - by an indirect mechanism, naturally - keep HIV particles viable by stopping them from crushing each other in the ejaculate. Just a thought, anything is possible in AIDS science.
Harris then turns his sights on the section in my original paper in which I explained how it came about that retroviruses were long suspected of causing cancer. He says:
"This is, in general, untrue. Not all cancers were blamed on viruses. Many viruses, such as FLeV, FIV, SIV, and even DNA viruses with reverse transcriptase activity, like hepadnaviruses in woodchucks were proven experimentally to cause cancer in lab animals, and even in random source animals (pet store animals, such as cats) brought to the lab and given virus."
Is this an answer? Does this explain which cancers were thought of as being due to viruses and which not? I consider it decidedly sick of Harris to juxtapose cancers in woodchucks, pet store animals and cats with the ongoing curse of our age, real cancers of many kinds. Is he really so naive as to believe that the billions of dollars devoured annually by the NCI in the US alone was to deal with cancers in woodchucks and cats?
What is the point of making excuses now about the mass failure by the scientific community then, and to wax eloquent about some detail about HIV which he finds "elegant". The fact of the matter is that then, about cancer, as now about HIV, the fundamental science is wrong, and no amount of epidemiological soft soap "isn't it funny that ..." can rectify it. Moreover, he was not himself responsible for this fiasco, so why is he bothering to defend it. He has enough on his conscience with the present situation.
The War on Cancer declared by President Nixon on 23/12/1991, based on the notion that viruses cause cancer implied that all cancers are caused by viruses, for one thing because those researchers who did not accept this were ignored and de-funded. It is a gross deception, like everything to do with HIV and AIDS is in our time, to say otherwise. To grasp what was produced in a test-tube and what is still being produced in them, I strongly recommend reading the paper by Peyton Rous (J Exp Med, 1911, 13, 397), especially noting his comment:
"The first tendency will be to regard the self-perpetuating agent active in this sarcoma of the fowl as a minute parasitic organism. Analogy with several infectious diseases of man and the lower animals, caused by ultramicroscopic organisms, gives support to this view of the findings, and at present work is being directed to its experimental verification. But an agency of another sort is not out of the question. It is conceivable that a chemical stimulant, elaborated by the neoplastic cells, might cause the tumour in another host and bring about in consequence a further production of the same stimulant".
The ludicrous situation in which contemporary cancer research has maneuvered itself into is described by Gerald B Dermer, who provides the evidence that cancer in vitro and cancer in vivo have nothing to do with each other.
So let us look in some detail at what Harris thinks is an isolation of HIV (Virology, 1992, 189, 695). It bears the inauspicious title "Factors underlying spontaneous inactivation and susceptibility to neutralisation of Human Immunodeficiency Virus", which rather suggests that it is not a very stable entity, as indeed it isn't. So unstable, in fact, that it disintegrates spontaneously.
What one then sees on page 700 is nothing other than a preparation of the above mentioned cellular particles, which are of different sizes and shapes, and, as the caption clearly states, are contaminated with "membranous residues" and "macromolecular fragments". This is not what an isolated virus preparation should look like. What they should look like can be seen in any virology textbook (and shown in Continuum). When real viruses are isolated, they do not need "fixing", which means embedding them in a resin to stop them from falling apart, nor slicing into ultra-thin sections to show up detail, only then being in a fit state to be photographed in an electron microscope. Isolated virus preparations should contain no impurities, and after staining in one piece to give contrast, are ready to be photographed. All particles should look alike. All viruses that are real, have been isolated and photographed in this way. The reader, open-minded AIDS researchers and especially Steven B. Harris could do worse than look at the publication about a virus in whose isolating and characterisation I myself was involved in (Virology, 1995, 206, 1, and Continuum).
Harris gets himself into deep water by trying to come to grips with "hard" science by questioning my contention that the correct characterisation of viral proteins has not been performed.
What is needed are photographs of the native gels of the proteins and of the nucleic acid, so as to prevent the skulduggery, as we shall see.
Harris thinks the missing proteins of HIV are found in the Cohen et al paper. But all that we see there is more fiddling and tinkering with the evidence, which in a criminal case would land him in prison for suppression of material evidence. We see the result of radiolabelled SDS (detergent) polyacrylic amid gel electrophoresis (PAGE). One needs to see the proteins on the SDS gel before antibodies to it were formed and radiolabelled. If you have something to show, and above all if you want to prove that the proteins of a virus have been isolated and separated according to size, then the native gel has to be shown before further experiments are conducted. This is standard procedure - except, of course, in this case where it really matters! If you attempted this with HIV isolations you would find that many proteins wouldn't fit in with the conventional HIV model. To get round this problem, only photos of certain antibodies which bind to selected proteins are shown, and the other proteins, which remain unbound by antibodies is not revealed. Only selected proteins are made visible by binding to antibodies, because only pre-selected proteins are used to inoculate experimental animals which are used to produce, with which these proteins are detected. The same applies to humans in whom only antibodies to proteins are produced with which they had previously been in immunological contact, i.e. inoculated with (except rheumatism and autoimmune disease). It is quite a difficult argument to follow which will leave many a head spinning, but that is how AIDS science works.
Variations of an original error (Ratner et al.) may enchant Harris, but remain an error just the same. They show once again that something has been obtained from the cell soup, not from a virus.
Harris goes on to explain that the evidence that the knobs attach HIV to cells is "massive", as if he had the requisite training to evaluate the evidence.
The evidence of 100,000 papers on HIV and AIDS should indeed be massive; unfortunately (or rather, mercifully) not one of them contains any direct evidence for the existence of HIV nor of its components. What is required is a standard isolation experiment, not something fanciful like sprinkling cloned DNA on to cell cultures and seeing what happens.
That they throw some mouse genes into cell cultures and produce something mouse-specific, is just modern alchemy. That resistance to antibiotics is also been bred in, transgresses against all scientific decencies, paid for by us, the taxpayer. Such misuse of public money is quite appalling. How can it be justified? It is scientifically unacceptable to dream up explanations of what went wrong, and proceed as if nothing of significance had happened, as is usually the case in AIDS "science".
We now join Alice in Wonderland in which Harris explains in greater detail how this "science" works, to wit, the concept of "co-purification", hitherto unknown to science.
He says "these are the same proteins which are coded for by the viral genome, and which co-purify with the infectious virus on sucrose gradients, as noted above. Why does it take a stretch of the imagination to image that they are viral proteins?"
Answer:
Something that co-purifies with something else is of no interest to anyone. Individual proteins should have a density that is entirely different to complete viruses, and should for that reason not band at the same density as viruses! It seems that these researchers have never even learned the ground rules of cell biology and virology. The quality of evidence that convinces Harris is frightening.
To try once more: second and third generation tests use synthetic proteins, clearly therefore they are not viral. How can something that is synthesised be viral. A virus is a creation of nature. Their use is an attempt to maximise reproducibility. Is that really so difficult to understand?
We now come to various observations where Harris finds it expedient to act dumb. In my original paper I quoted from the instruction leaflet accompanying one test kit, namely,
"The test for the existence of antibodies against AIDS-associated virus is not diagnostic for AIDS and AIDS-like diseases. Negative test results do not exclude the possibility of contact or infection with the AIDS-associated virus. Positive test results do not prove that someone has an AIDS or pre-AIDS disease status nor that he will acquire it" Harris feigns incomprehension. The significance of it is that the manufacturers are aware of the difficulty of interpreting any result, because from experience they know any number of conditions unrelated to HIV/AIDS can test positive, equally that people can test negative and "indeterminate", yet still develop AIDS. Harris then goes in for some face-saving goal post moving by introducing the novel orthodoxy that not all HIV-infected people develop AIDS.
I originally observed that some HIV researchers have tried to circumvent the problem by pointing to something called "direct" evidence for the virus. All that this meant, though, was arbitrarily selecting a protein of a certain size which happened to coincide with that shown in HIV models. The delusion of such "evidence" was illustrated when the protein later turned out to be of human origin!
to which Harris answered: "neither gp-160 nor the viral reverse transcriptase of HIV (which is magnesium dependent, unlike any in your cells) are of 'human origin'. You will find none in any human cell uninfected with HIV. Both are coded in the genome of HIV".
p24 is the direct evidence for HIV as far as most HIV researchers are concerned. Steven B. Harris tries to distract attention by using reverse transcriptase and gp160, which have never been considered in this context. gp160 is nothing other than a cellular precursor protein, and the famous reverse transcriptase is not even correctly demonstrated, because the RNA template used for this is readily converted into DNA by cellular DNA polymerases. The magnesium ion argument, therefore, is just another damp squib.
If reverse transcriptase were really proven, which is questionable given the lamentable state of AIDS research, then it would have to be encoded the special cell lines need to make HIV. Where's the problem?
We now come to one of the 3 essential points of my paper, namely, to explain what actually happens when they try to prepared HIV. Harris dismisses it as "a sorry tale" and "baloney". This is hardly an answer, though I appreciate that it is all he can do. It is pretty obvious that Harris's grasp of all of this is pretty tenuous, and a successful rebuttal, if there were one, is well and truly beyond his grasp of the subject. Since I consider the AIDS disaster is anything other than a joke, I can only advise him to put a cold towel over his head, check out my references, and come up with a better answer.
Needless to say Harris's standing does not rise in anybody's eyes when he has to rope in Gallo's problem to help him out. How fatuous to rebut one non-existent virus with another non-existent virus. Does he really think Gallo didn't prepare HTLV-III but did HTLV-I? It is surely obvious to everyone by now, that Gallo has never done anything right in his life. Has Harris not read the Crewdson Report in the Chicago Tribune; is he unaware of the Office of Scientific Integrity's findings; is he not aware that Gallo has finally got the push from the NCI? Yet he has the nerve to bother people with some problem Gallo may have had cooking the books.
What an insult of an answer for Harris to waffle on about cross-reacting sera. If one does not know the answer to a problem, the correct answer is to say "I don't know". No-one can adjudge a technical problem on a highly specialised subject not in his field. Flu vaccines, hepatitis B and malaria all cross-react with HIV tests; whether a horse virus nobody has heard of nor cares about, also does so is about as relevant as the price of tea in China.
It is perfectly understandable that Harris has difficulty in rebutting the template switching and hybridisation arguments put forward in my paper. I am a virologist, and this is pure virology. Does he think I woke up one morning and said to myself "let's play silly buggers, and put it about that HIV didn't really exist." Of course not. No doctor could possibly rebut it without the help of a top-rate virologist. If a Duesberg tried, I'd pay attention, but talk of sera and antigens, what next! Harris then gets carried away rather by his own rhetoric in saying "actually, one cannot help asking why nobody has spotted the flaw in Lanka's argument, which suggests that "HIV DNA" must be in every normal cell, since HIV as a separate entity does not exist, and therefore no DNA PCR test can ever be "negative" on anyone. Yet these tests routinely find no HIV DNA in HIV negative people."
One major difference between what I have suggested and what the AIDS-Establishment blithely accepts, is that the former is a working hypothesis offered in the spirit of true scientific endeavour, subject to revision and intelligent criticism, whereas the latter is totally failed dogma.
It is my humble opinion that the sequences are endogenous, and anybody can prove it. Not only in man, of course, but also in the special cell cultures that always have to be used to make HIV. But here's the rub, dear Dr. Harris! That is how HT23 (the first human retrovirus) was discovered in 1975, but which Gallo very soon thereafter had to withdraw from the "market", because vociferous ape virologists staked an earlier claim to it. This also explains why Gallo and Montagnier published almost identical sequences, because he had purloined them as endogenous sequences from Montagnier; only illicit collusion could have produced the concordance that was obtained. Not only between these two, but also between Robin Weiss, although the Pasteur Institute has up till now not sued him for patent infringement. The evidence is available at the Patent Office in London for all to see.
One reason why in the so-called PCR controls nothing is found, is that the human cells used to act as controls, are not stimulated (stressed) in the same way as those in which one wants to detect HIV, ie. they don't compare like with like. The RNA detected in PCR tests is not expressed under normal conditions, because they do not belong to the normal repertoire of nucleic acid. The RNA detected is formed in response to stress when cells in short term cultures begin dying, or are treated in such a way that its cellular activity is disturbed, and "retroviral sequences" are expressed which are not formed (transcribed) otherwise.
PCR only detects very short stretches of DNA that in this case are supposed to be components of the genetic material of viruses. If one succeeds in this, it is immediately described as "PCR positive", implying that the remainder of the genetic material ascribed to HIV, is found somewhere else. This is pure guesswork!
On careful reading of Harris's references on PCR and many others, one discovers that a number of PCR tests for viral RNA use chromosomal DNA as controls! As every genetics student would object immediately, this can't be done. Transcription into RNA changes the gene sequence, ie. the RNA is "edited"; on reverse transcription back into DNA it is no longer the original DNA.
Starter molecules needed for this edited DNA are now prepared which fit this DNA, but not the original. Herein lies the wizardry! A wonderful piece of deception, and available for all to see! All recounted history! Regrettably, with terrible consequences. The argument is tricky, and if Harris can't or is reluctant to grasp it, then so be it. I have never claimed that HIV DNA is present in every human being, for the obvious reason that it doesn't exist except as a lab construct.
Harris asks:
"then why does a positive test give you a 50% chance of dying of immunodeficiency in 10 years? That's a harsh punishment from rheumatology and sunbathing. And why do positive antibody tests correlate so well (both positively and negatively) with viral culture tests (which measure a protein) or with direct PCR (which measures DNA)."
Answer:
I presume Harris means "have a 50% chance of dying of AIDS not immunodeficiency". Or does he not know that they are not synonymous, given some of his silly pat answers, I think he's not sure? Only 39% of AIDS cases have anything to do with immunodeficiency. It appears to be all the same to Harris. HIV kills off T4 cells, therefore 10% of people get Kaposi's Sarcoma, 6% develop dementia, 3% develop lymphomas and 19% waste away.
Or is this the point at which the "fiendishly clever" effect of HIV comes in, whereby it causes these totally disparate diseases "indirectly", by molecular mimicry, by apoptosis, by autoimmunity, by protein toxicity? If Harris knew anything he'd know that he knew nothing: immunology is essentially still in the Dark Ages, scarcely more advanced than mechanics was without Newton.
By the way, is it another slip-up by Harris saying "have a 50% chance of dying"? Is this now official policy - only half the HIV positives develop AIDS? Since when, and why, or is it really 90% as he states further down? Or don't all people with AIDS ultimately die?
Harris asks:
"if there's no virus to explain all this, how does Lanka explain it? Remember, one must explain not only why people who test positive for "HIV" antibodies almost always test positive for HIV by culture and PCR (which don't test for antibodies), but also why people who test negative for antibodies test negative by culture and PCR (see last set of 4 papers quoted)".
Answer:
Thank you, Dr. Harris, but I do not need lessons on what constitutes a proof in science. That you suddenly let on that you know, too, makes me wonder why you have been so complacent in all your "proofs" up to now.
I suppose I do have to spell it out, superfluous as it seems. It is not disputed that "HIV positives" are in some way at risk. The question is how and of what.
I strongly urge readers to study carefully the papers cited by him to understand why, in HIV negatives, PCR is also apparently negative. It is quite simply because they never compare like with like, and play a dirty trick on top of it all. The first HIV PCR studies gave no concordance at all between antibody and PCR tests. Nowadays, this is glossed over, and in those cases where this can't be done, it is claimed that HIV is present only in the mutated, defective or non-integrated form. In summer 1993 (see my original paper) they invented the concept of "molecular mimicry" to explain the inexplicable: it says that the virus has mutated so much that in effect it has mutated itself out of existence.
Harris's claim that "HIV is the only variable which independently correlates with AIDS risk in all AIDS groups. None other has been found."
Answer:
The first howler is for him to assume that AIDS is the same disease in all groups. It isn't! How many IV-drug addicts have Kaposi's sarcoma? Which gay man has invasive cervical cancer? Is Harris not aware of the 1994 CDC announcement that there cannot have been any HIV in Factor 8 given to hemophiliacs, since drying of blood products reduces the risk of infection to "essentially zero". But enough of such crass question begging answers.
I am aware of Harris's dismissal of the alternative drug intoxication theory. I assume he is relying on the Winkelstein et al. paper, and no doubt assumes that is the end of the matter. I can only rejoin that if he is so naive as to rely in any way on the accuracy of self-reported drug use - just as an aside, who the hell knows what people really take in when shooting up, swallowing or sniffing adulterated illegal drugs prepared in back street labs? Has he never been in an organic chemistry lab and noted the nasty reagents that are used and the residues and side reactions, if so he would be less cocksure.
The other - oh, so hard to quantify, so let's forget all about it - factor is the effect of a psychological death sentence of a positive diagnosis. As a virologist I cannot either, but as a human being I know it to be extant, and I cannot just forget about it as Harris seems to with such insouciance.
Harris:
"There is no evidence that these drugs (AZT and its analogues) produce deficits in the cell-mediated immune system which are important clinically. There is no evidence that they produce AIDS (as Lanka may be trying to suggest here) and a great deal of evidence they don't (the Concorde trials)."
Answer:
If Harris had any understanding of chemistry and were altogether less intellectually dishonest, he would know that AZT was designed to kill cells indiscriminately. He would take the trouble to find out how it does so. He might also have read the book by Nussbaum "Good Intentions" which chronicles in great detail the shenanigans, whereby AZT was resurrected as an "anti-viral" when previously it was cytotoxic. He would also then realise that misguided gay rights agitators were responsible for this horrendous state of affairs, for which they and a whole lot of completely innocent people are now paying the price. He would then realise that AZT cannot by waving a magic wand (serendipitously?) help AIDS patients after all, say, the way a natural product like aspirin, jojoba and primrose oils, just might. If he, further, had any grasp of pharmacology, he would know that different people manifest different degrees of drug absorption and drug metabolism. And just a little thought on his part would tell him that if you reduce the dose of even a toxic drug to a low level, no harmful effects might be manifested. He might also realise that people don't always tell the truth, and flush nasty things down the toilet.
Dr. Harris is pretending that the immune system is properly understood. I hazard a guess that at most 1% of what it really comprises is known, hardly a proper basis for dogmatism. Least understood is the significance, if any, of T-cell counting. Harris would get the most up-to-date critical review of current knowledge on this troubled subject by reading Eleni Papadopulos-Eleopulos et al. in Genetica, April 1995. And when he has done that he would benefit by swatting up on the whole murky topic of antibody testing and PCR in Bio/Technology, June 1993, by the same authors. He will become a wiser man.
I know someone who has for several years had only three T4 cells, which he named after his dead friends. He himself is well. Dr. Felix Konotey-Ahulu of the famous Cromwell Hospital, London, has described a tribe in Ghana whose average T-cell count is only 100!. Also, why can an individual have twice as many T-cells in the morning as in the evening? Is this also "just baloney". Certainly not, it is all well documented. These arguments are all just conjecture, and only tangential to the question whether HIV exists or not and how it was "manufactured"; dealing with them thoroughly would open up a whole new can of worms, beyond the scope of this response.
Harris denies that up until recently, being HIV positive did not constitute a definitive prognosis of death. Since when is it "official" that 10% of positives will be alive after 15 years? I thought you said it was 50% (earlier on, remember?), or is that to be understood as meaning 40% die in years 10 to 15? In German, there is a saying "Luegen haben kurze Beine" (lies have short legs, ie. they don't get you very far). Stop making policy on the hoof, it won't work. Long-term survivors have only been officially recognised for the past 2 years, now you claim they are recognised to constitute 10-50%.
Harris wobbles uncertainly around what AIDS diseases are. Destruction of the immune system, eh? Dementia, cachexia, lymphomas and Kaposi's sarcoma. Remember, "Luegen haben kurze Beine."
Despite the flawed nature of Dr. Harris's response, I would nonetheless congratulate him on a creditable effort. It surpasses by far anything that I have ever come across before, and contrasts sharply with the lamentable position of most AIDS scientists who are satisfied with the statement: "the evidence that HIV causes AIDS is overwhelming, though we still don't know precisely how."
The correct position is that the evidence which is there is none, and absolutely nothing is known about how it is supposed to do so.
ADDENDUM.
In his impressive SKEPTIC article, in which he satisfies himself that there are no causes of AIDS other than HIV, he nonetheless blows the whole gaffe by reaching the following two conclusions:
That AIDS will not spread beyond its present (tiny) risk groups.
That AZT has no useful function.
He seems not to have realised that he has thereby taken the ground from under the whole AIDS construct, for, were it not "official" that AIDS can afflict anyone, the enormous public funding for AIDS research ($96 annually per heart patient vs. $36,000 per AIDS patient) would not exist; and equally, if the vast profits accruing to Wellcome through AZT fell by the wayside, the whole edifice of direct and indirect funding of HIV research would grind to a halt. As Kary Mullis observed a while ago "who wouldn't be infinitely fascinated by how HIV causes AIDS if there is a $2,000 million price tag attached to the question every year". As an assiduous student of epidemiology Harris might ask himself, why has HIV not spread, as according Farr's Law it should have done?