sealamp
2003 is not the 1950s. We have much better tools at our disposal, namely the entire field of molecular genetics.
Please explain how someone could be PCR positive for HIV and uninfected.
Roger_Mexico and trueskeptic
If you think that a virus needs to be isolated in order to show an antibody test works, you are mistaken. Protein purification is sloppy. Virus purification is even worse. The cleanest way to make an antibody against a protein is to clone the gene, transcribe/translate it in either an ectopic cell culture or an in vitro system, and use that to make the antibody (either monoclonal or polyclonal).
Let’s say you have your virus in a tube. a) How do you know it is your virus? b) How do you know it is pure? c) How do you know what is in that virus? These are three big questions which take years to answer. They cannot be answered in individual studies, and they haven’t. Having a pure virus means little. Having a picture means even less.
I don’t understand the fixation on isolation. First, HIV has been isolated hundreds of times, and can be part of the diagnositc algorithm. Second, morphology has little to do with classification. The reason HIV looks globular on EM is because it is surrounded by a phospholipid envelope. HIV emerges from the cell by taking a bit of cell membrane with it. What you see on EM is that cell membrane, which obscures the virus. This is pretty evident in pictures like this. (Sorry the image is massive).
I can’t possibly imagine how seeing “buds” on an EM gives any credence to the fact that HIV causes AIDS. How do we know HIV is a retrovirus if the morphology is obscured? By its behavior: Montagnier and Gallo are pretty clear. They fractionated T-cells from a patient with AIDS, and found a fraction which had reverse transcriptase activity. This enzyme is only found in retroviruses, and nowhere else in nature. This fraction had proteins similar with other human T-cell leukemia viruses, but was different in a number of respects. It was named HTLV-III, later HIV.
20 years of work led to better isolates, better culture conditions, better characterization of the structure, lifestyle, and lifecycle of the virus. The mechanism of HIV infection, propogation, and CD4 depletion was chronicled in tens of thousands of papers. This is how science is done. It is a big jigsaw puzzle being put together by thousands of highly intelligent people. If the puzzle starts out wrong, the pieces don’t all fit together and somebody notices. If there are errors in assembly along the way, they are corrected. HIV researchers have made errors, for instance in the efficacy of AZT monotherapy. Those errors were corrected, because others noticed.
20 years has also shown us that specific treatment of the retrovirus completely reverses the disease. Nobody could ask for better evidence than this.
About all of those papers listed and peer-review. 1) Drop out all of the letters, correspondence, commentaries, and reviews. Those aren’t peer reviewed. 2) Duesberg is a member of the National Academy of Sciences (from work he did on aneuploidy), so he is entitled to publish in Proceedings of the National Academy of Sciences without peer-review. 3) I do not see a single research article in a higher-tier journal. The only peer-reviewed journal I see up there is Genetica, which appears to be geared for fast review. I am in genetics, and I have never read or even heard of an article outside of HIV dissent in this journal. Its impact factor is extremely low and I would not hold it past them to publish provocative stuff just to get people to pick up a copy of the journal.
So, going through the list. E. Papdopulos-Eleopulos has absolutely no peer-reviewed primary research on HIV. 13 cites are listed in PubMed. Most of his/her stuff are reviews (8) and letters (3). There are two published in Medical Hypotheses, a journal devoted to publishing hypotheses that aren’t necessarily supported by any primary data.
R.S. Root-Bernstein has 11 cites. 4 are reviews, 2 are letters. The other 5 are published in either Med Hypotheses (3) or The Journal of Theoretical Biology (2) (need I say more).
G. T. Stewart has 16 cites. 2 reviews, 11 are letters or correspondence. The remaining 3 are policy, not research, articles.
Duesberg has 29 listed. 8 are reviews, 17 are comments and letters. The remaining 4 are the primary research that we so badly want. 1 is in PNAS (an epidemiologic study that has won a world of criticism), 2 in Genetica (one on AZT toxicity in cell culture, one is a re-analysis of the San Francisco Men’s Health Study). The last is a recently published article in J Biosci (which previously was the Proceedings of the National Academy of Science of India) on the chemical bases of the various AIDS epidemics. It is available free online. For all of the shooting at the HIV-AIDS community’s science, maybe I’ll shoot at this one. I bet it won’t be that hard.
So you have 3 peer reviewed research articles. 1 non peer reviewed primary article. Add 6 theoretical articles or hypotheses with or without primary data. That’s a helluva lot of noise for people who cannot seem to find much data to support their hypotheses. Or at least they are being “suppressed” by the “good old boy system” that keeps “genius thinkers” “down.” For all of the criticism of their science-by-news-conference that Gallo did (he published the results, peer reviewed, in Science in May 1983, BTW), the HIV dissent sure practices a lot of science-by-website.
Sticking HIV alone into PubMed brings back 130,208 hits. 16,507 of these are reviews. 10,404 of these are correspondence. 177 are in Medical Hypotheses, 55 in J Theor Biol. So we have 4 (including the PNAS one) versus 103,061 articles.
Next, about detection. We can, and have, gone round in circles about the ELISA. Your issues with the ELISA just don’t hold water. Every clinician out there knows that the ELISA gives huge false positive rates – it has horrible specificity. It is cheap, though, and it is very sensitive. That is why an ELISA positive by itself means next to nothing: it must be confirmed either by Western or by PCR. Don’t keep pointing out the false positive rates of ELISA in dogs or dialysis patients. We are quite aware of these, and that is why we don’t make clinical decisions based on it.
One other point. This has gone on too long, so I’ll be snappy. trueskeptic points out that HIV genomes are over 5% different, and the Perth group doesn’t believe they are all the same virus. This conveniently ignores the fact that reverse transcriptase has a very high error rate, so HIV has a high mutation rate. This one fact in itself explains many clinical aspects of the disease: why a triple replication blockade is necessary to prevent mutations for drug resistance, why >90% drug compliance is absolutely required to prevent resistance, why attenuated viruses for HIV vaccines may be a Very Bad Thing, why a vaccine is not easy to make work (a vaccine triggers antibodies against a specific viral antigen; all viruses with that antigen get killed; this puts strong selective pressures on viruses with mutations in the antigen), why HIV has such a low virulence. The list goes on, but I will stop.