Re: Questions for Christopher Noble & Nicholas Bennett 14 September 2004
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Nicholas Bennett,
Infectious Disease Postdoc/Clinician
Department of Pediatrics, University Hospital, Syracuse NY

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Re: Re: Questions for Christopher Noble & Nicholas Bennett

Mr Russel asks for several points, to which most of my answers are, initially, why?

As a Philosopher, Mr Russel is no doubt aware that a great many problems (God, Morality, Existence) cannot be solved in a concrete fashion. There are degrees of certainty. He is perhaps mistaken in thinking that "hard" science is any different! Even the ubiquitous "statistically significant" p-numbers are a measure of chance. p<0.05 merely means that there's less than a 1 in 20 chance the results are a fluke. That means that 1 time out of 20 you can EXPECT to get "statistically significant" results from any random trial!

But I digress...

1. HIV serostatus has been shown to be predictive of immune failure, as judged by lab markers (CD4 cell count) and clinical status (the occurance of opportunistic infections). No other risk factor has been shown to have such a strong correlation, and no other risk factor is a risk IN ISOLATION. There are however several risk factors that will predispose any one individual to acquiring HIV or progressing to AIDS. Any sensible person would conclude that "The most likely cause of AIDS is therefore HIV".

There are clearly going to be cases where HIV serostatus doesn't result in a progression to AIDS, and a minority of HIV+ people are long- term non-progressors. Since these people tend to have stronger anti-HIV immune responses, or gene deletions or changes that impair the virus, or mutated virus itself, these all actually SUPPORT the idea that HIV causes AIDS.

So HIV does seem sufficient to cause AIDS in most people: at least except in rare cases no other risk factor has been shown to tip the balance from HIV infection to clinical AIDS (the exceptions I'm aware off are, ironically for Mr Russell, second HIV infections with another virus!).

The most important fact is that several studies have looked SPECIFICALLY at the issue of drug use (especially poppers) and their role in causing AIDS. Contrary to the "logic" used by many of the AIDS dissenters, there is no clinical proof that poppers in any way influence the immune decline seen in AIDS. In one study in fact, CD4 T cells were higher in the drug-use group! Far from KS only being seen in those with popper use, it is in fact no different in rate in users or non-users. This is a myth promoted by those keen to refute the HIV/AIDS paradigm, for whatever reason.

2. Why must we have EM confirmation of virus from semen and blood? Why won't PCR, antigen, or virus culture suffice? After all, virus culture is used routinely for many viruses in the clinical setting. I have posted a message here before stating that virus titres in blood may be far too low (by 4 orders of magnitude) to have a realistic attempt at direct EM, at least not without a drastic overhaul and reinvention of the isolation protocols. I imagine semen may be just as difficult.

3. Sexual transmission was originally implied by noting the appearance of HIV in one particular sexual risk group. That has subsequently been confirmed by many series of contact tracings and epidemiological studies. HIV has behaved much as would be predicted for a sexually transmitted virus first appearing (in the West) among homosexuals. It was largely confined to that risk group and then has subsequently spread to the heterosexuals, IV drug users, and various blood -product recipients. This is entirely consistent. How would Mr Russell propose we confirm sexual transmission: does he think we can isolate and sequence EVERY case that comes to light and compare it to their risk contact? In fact, it was contact tracing of "low/no risk" subjects that linked them to high-risk patients through a sexual route. Sexual transmission is the most likely explanation in that situation.

4. What gold standard for antibody detection would Mr Russell like? HIV PCR or culture has confirmed HIV infection in most or all HIV+ people, depending on the efficiency of the system (another example of where science isn't as "hard" as some would like to think). Believe it or not, sometimes you stick some bacteria or virus in a culture flask, and it won't grow. To read experiments where they have managed to get several thousand tissue-culture infectious doses (TCIDs) from a single teaspoon of blood, that highlights the amount of HIV in the system, if you have the power to look for it. (Note that the HIV was mostly in infected cells, and therefore could not be found by EM without secondary culture outside the body: these experiments have been done, but are ignored by people like the Perth Group).

Mr Russell states that:

"If you cannot answer one or all of these questions then your hypothesis that 'HIV' exists and causes 'AIDS' falls."

This is a straw-man argument: one where false logic is used to set up a situation that can then be refuted at leisure. The proposals Mr Russell presents aren't consistent with standard scientific practise. In particular he asks for "one main experimental study", somehow encompassing the skills of contact tracing, virus isolation, EM, protein analysis, genetic analysis, cohort studies, prospective, longitudinal and cross- sectional studies and covering all available and future confounding factors. Not possible.

I can however provide one, single reference to cover all of the above.

Fields Virology, 4th Edition. Chapter 60 (volume 2). It has 618 references contained within it: THAT is how we know HIV causes AIDS.

Competing interests: None declared