It's very difficult to grasp the issues involved in the AIDS dispute. However, I've stumbled across the clearest exposition I can find here:
http://www.ourcivilisation.com/aids/hivexist/
It's a longish interview with Dr. Eleni Papadopulos, a prominent sceptic, which rewards close reading. She defines what a retrovirus is, which helps. Prior to the discovery of retroviruses, it was assumed that DNA always produced RNA which in turn went on to produce proteins. However, retroviruses are a class of virus containing RNA that generates DNA that goes on to sit within the host cell genome:
ELENI: Yes. Another important point is that retroviruses do not directly use their RNA blueprint to make more virus. According to retrovirologists, what sets them apart from nearly all other viruses is that retroviruses first make a DNA copy of their RNA. This DNA then moves into the cell nucleus where it becomes part of the cellular DNA. This stretch of DNA is called a provirus and there it sits, hibernating, perhaps for years, until something activates the cell.
CJ: What happens then?
ELENI: The proviral DNA is copied back into RNA and it is this RNA, not the original RNA, that instructs the production of the necessary proteins to make new virus particles.
CJ: Why are they called retroviruses?
ELENI: Because for a long time biologists believed that the direction of information flow in the cells of all living things was from DNA to RNA, and thence to the proteins whose synthesis the RNA instructs. If we say this direction is "forwards" then what retroviruses do first is copy their information "backwards".
CJ: Understood.
ELENI: There's one more thing. One of the proteins inside a retrovirus particle is an enzyme which catalyses this process. Not surprisingly, it's called reverse transcriptase*.
*RT--my comment
CJ: And that's it?
ELENI: Well, that's why they're called retroviruses.
There's something that would prove the existence of a retrovirus and the linkage of that to a specified disease. It utilises a sugar solution gradient that is spun a high speed in an ultracentrifuge. Particles from host tissues placed in this solution eventually come to be banded at a place within the gradient that matches their own density. The band for retroviruses is at 1.16 g/ml.
Then, you'd need to get electronmicrographs of the particles in the 1.16g/ml band, and they'd have to be within 100-120nm diameter and be covered with knobs:
ELENI: Gallo and all other retrovirologists, as well as Hans Gelderblom who has done most of the electron microscopy studies of HIV, agree that retrovirus particles are almost spherical in shape, have a diameter of 100-120 nanometres and are covered with knobs. (12,13) The particles the two groups claim are HIV are not spherical, no diameter is less than 120nM, in fact many of them have major diameters exceeding twice that permitted for a retrovirus. And none of them appear to have knobs.
Next, you'd need to extract a sample from the band and show that the particles could replicate. You'd also have to show that the replicated particles could cause the disease/effect in question.
The article was written in 1997, and prior to that time, something like this had never been applied to HIV. However, when centrifugation was attempted by the two groups mentioned in the snip, none of the particles in the 1.16g/ml band conformed to size expectations for a retrovirus, and in any case, no knobs were seen. Nor, as far as I can see, was an attempt made to show the particles could replicate--for example, by using the replicants to re-infect uninfected host cells, and from those, collecting samples that could have in turn been centrifuged to establish unequivocally the presence of a retrovirus.
The assumption that HIV causes AIDS is indirect: it depends on establishing the presence of antibodies to the presumed HIV retrovirus. All the tests depend on this. But the inconvenient fact is that many processes can generate such antibodies, including those that might occur in people who do not have AIDS.
Papadopulos doesn't deny that the "HIV" test is useful:
CJ: Then is it fair to say that the HIV antibody tests are useless?
ELENI: No, they're not useless. There is no doubt being in a risk group and having these antibodies is not a good thing.
CJ: How can that be?
ELENI: Because empirically such people are more likely to develop the illnesses we classify as AIDS. (31) In fact, there is evidence published in the Lancet that a positive test also predicts increased mortality from diseases which are not classified as AIDS. But what the tests don't do, or at least there is no proof that they do, is prove HIV infection. Or even less that HIV infection is the reason people develop AIDS. You may not appreciate that the only evidence HIV causes AIDS is these tests. If the tests are unproven for HIV infection then there is no proof that HIV causes AIDS. (3, 4, 5, 26, 32, 33, 34)
CJ: What about a positive test in people who are apparently healthy and not in any risk group? Should they be worried?
ELENI: There is no data to answer that question and I think it would be impossible to ever obtain that data. There would have to be an experiment comparing matched groups of healthy people with and without these antibodies. In other words, follow people with a positive test over a period of years and see who developed AIDS and who did not. The trouble is it would be very difficult for most people knowing they are HIV positive, as well as their physicians, not to believe that sooner or later they're going to get very sick and eventually die of AIDS. And that mindset may greatly effect the results of such an experiment. From both sides.
CJ: What do you mean from both sides?
ELENI: I mean that patients' health will be affected knowing they are HIV positive and their physicians will feel compelled to offer treatments with drugs given in the belief they are necessary to kill a virus the patients do not have.
CJ: The drugs themselves might be harmful?
ELENI: Well AZT, the original and still most widely used drug is certainly well known for its toxic effects and in fact some of these effects mimic AIDS.
CJ: What if we did this experiment, and we did it blind, and found that the HIV positives were more likely to develop AIDS than the HIV negatives? What would that tell us?
ELENI: On our present data that would mean the same it means in the AIDS risk groups. Gallo and his colleagues serendipitously discovered a test which for some reason predicts a tendency to get sick from certain diseases that are lumped together as AIDS. But it doesn't prove that the link to all these diseases is a retrovirus. That can never be proven unless HIV is proven to exist by isolating it first and then used to validate the antibodies as HIV antibodies. Even then, you can't say HIV causes AIDS just because it's present in AIDS patients. Association doesn't prove causation. You can be present at a bank robbery but not be the robber. You need other data to prove causation. In fact, according to the CDC AIDS definition, you don't even need to be HIV infected to be diagnosed as AIDS.
CJ: That sounds really crazy.
ELENI: It's written down in the literature. Under some circumstances the CDC AIDS definition requires a patient to be diagnosed as a case of AIDS even if the patient's antibody tests are negative. (35)
CJ: What about the RNA tests. The PCR and viral load and like?
ELENI: That's another huge subject but I can say just one thing. All these tests rely on matching a piece of the patient's RNA or DNA to a test piece of RNA or DNA deemed to originate from a particle called HIV. You can think about this like the rabbit antibodies. There's another bottle on the shelf and the label on this one reads "HIV RNA". But if a retroviral particle hasn't been isolated and purified and shown to be a virus, how does anyone know where this piece of RNA comes from? The HIV experts themselves say that there are about one hundred million distinct HIV RNAs in every AIDS patient. (36)With that much variation one would think that a virus is the most improbable source for such RNA. I mean, how can a virus have that much variation and still be the same agent? Still make the same proteins and induce the antibodies? Still perform all the same tricks?
CJ: Tell me Eleni, if there is no virus where do all the things Montagnier and Gallo found come from? I assume you do believe they did find something in their cultures?
ELENI: Of course they found something. They found many things. All the things we've discussed. And your question is fair. In our view it is possible the RT and particles could be some reaction produced when cells from sick people are cultured. Or the result of the chemicals introduced into the cultures. We know that both normal and pathological processes can be associated with the appearance of retroviral-like particles. There's absolutely no doubt about that. What exactly are all these particles? Well, some may be no more than pieces of disintegrating cells. Others certainly look more uniform and might conceivably be viral-like or even retroviral-like but in the context of HIV what really matters is proof that at least one of these varieties of particles is a retroviral particle. Even if we had that proof, the RT and the particles and proteins could all come from an endogenous retrovirus.
CJ: What's an endogenous retrovirus?
ELENI: Unlike the case for all other infectious agents, normal human DNA contains retroviral information which did not get there following a retroviral infection. The cell was born with it. So amongst all our DNA there are stretches made up of some retroviral information and that may sit there maybe all your life until something happens. The DNA starts to make RNA and hence proteins, and this may go even further and lead to the assembly of endogenous retroviral particles. They're called endogenous because they're not something that got in from the outside. Like HIV is supposed to. Something that gets in from the outside is called exogenous. Long before the AIDS era everyone knew that in animal cells endogenous retrovirus production could occur spontaneously. You make a cell culture and do nothing else. Just leave it on the bench for a few days or maybe a few weeks and then one day it starts to produce retroviral-like particles. They seemingly come out of nowhere and the process can be significantly accelerated and the yield of particles increased, sometimes millions of times, by conditions which induce cellular activation, the same conditions which are obligatory to obtain what is called HIV from cell cultures. Interestingly, up until 1993, neither Gallo nor Fauci who is another well-known HIV researcher, (37) accepted that humans contain the DNA to make endogenous retroviruses but now it's accepted that endogenous retroviral DNA forms about 1% of human DNA. For the record, that's about 3,000 times larger that what the experts claim is the size of the HIV genome. And what's more, new retroviral genomes can arise by rearrangements and recombination of existing retroviral genomes.
CJ: So HIV could be an endogenous retrovirus?
ELENI: There are many explanations for the laboratory phenomena held up as proof for the existence of HIV. We went into all these in a very long article we wrote for Continuum magazine last October. (38)
CJ: Can you tell endogenous and exogenous apart?
ELENI: No. Endogenously produced retroviruses are morphologically and biochemically indistinguishable from exogenous retroviruses.
CJ: If HIV is an endogenous virus, why would AIDS patients produce such viruses when we don't?
ELENI: Because the patients are sick. In fact they are sick before they ever develop AIDS. So their cells are sick and their sick cells find themselves in the right condition in cultures to be activated. That's what's needed to produce endogenous virus and that's been known for decades. Either the agents to which the patients are exposed induce the right conditions or the culture conditions play a part. Perhaps a major part. I don't know which contribution is the greater but that might have been sorted out a long time ago if the first HIV researchers had included a few control experiments.
Papadopulos' position, and that of many sceptics, is a highly nuanced one: it can't be characterised simply as "AIDS denialism". It has a strong scientific justification, and ought to be under open discussion. But she, and many others, find it very difficult to publish work, and when they do, it's often in less well-known journals because their papers get rejected by the more prominent ones on account of dogmatism.
I thoroughly recommend reading the whole of the article to get a better handle on the kinds of things sceptics are saying, and not relying solely on orthodox sources.