Does HIV cause AIDS?

Richard Burge R.Burge at bay.cc.kcl.ac.uk
Fri Jun 3 12:46:45 EST 1994

Maybe HIV doesn't cause AIDS. Crazy notion - or is it?

I was at a lecture a couple of days ago by Kary Mullis, 1993 Nobel 
Chemistry Laureate (inventor of PCR). He proposed a very interesting 
alternative hypothesis for the AIDS epidemic whereby AIDS may be due not to 
HIV infection as such, but due to infection by retrovirii or other infectious 
agents in general.

It goes something like this:

If you are infected by some pathogen every so often, your immune system leaps 
into action to deal with it (clonal expansion, lots of plasma cell division, 
that sort of thing). All well and good, but if one of the plasma cells 
involved harbours a lysogenic retrovirus (normally dormant, but replicates 
during cell division since it is incorporated into the chromosome), then you 
will produce lots of copies of the virus as an unfortunate byproduct of 
producing lots of plasma cells. That virus may be non-pathogenic in small 
quantities, but when your blood is suddenly awash with it, your immune system 
will attempt to destroy it, i.e. you will get two responses - one to wipe out 
your flu infection or whatever and one to wipe out the virus produced as a 
result of wiping out the flu infection.

Now, if you are reasonably healthy, not many of your cells will harbour 
a retrovirus. If, say, 50 of your million plasma cells (arbitary figures) have 
a retrovirus, you will only elicit an *extra* immune response if one of those 
50 is selected for clonal expansion, so you'll only put an extra strain on the 
immune system occasionally.

If *all* of your plasma cells harbour a retrovirus, then you put an 
extra strain on your immune system *every* time it deals with an infection. An 
immune response will lead to a second immune response, which will lead to a 
third immune response and so on.

Mullis suggested that this perpetual immune system activation resulted in 
breakdown of the immune system, i.e. AIDS.

This is not necessarily linked to HIV infection, since HIV alone may be 
completely non-pathogenic at normal levels. It is only it's synergistic action 
when present alongside hundreds of other infections that it becomes a problem. 
Even then, it is not HIV itself that is the problem, but the overall level of 

This increase in the number of non-pathogenic (if present on their own) virii 
in an individual could have arisen from the San-Francisco bath-house scene 
(lots of partners, lots of contact, warm & damp environment, lots of 
opportunity for infection), since if one individual caught something it would 
spread like wildfire. In such a scenario, AIDS may have hit the gay community 
first because they were more gregarious than the heterosexual community - 
heterosexuals with hundreds of partners who each had hundreds of partners who 
each had hundreds of partners would be just as likely to spontaneously 
initiate an AIDS epidemic.

In such a scenario, all AIDS sufferers would probably have HIV (along with 
anything else you care to mention), but not everyone with HIV will necessarily 
develop AIDS, since HIV alone is insufficient to cause it. Blood-to-blood 
contact would still spread AIDS because the blood of an AIDS sufferer would 
contain many, many *different* infectious agents. This would explain 
increasing CDC figure for the latency of the virus (what is it, 12 years or so 
at the moment?) since an HIV+ person may have no chance of developing AIDS 

This would also mean that money spent researching an anti-HIV drug is money 
down the tubes. An awful lot of governments may have been funding the wrong 
thing, but the scientific and political establishment has become blinkered - 
too much money is now at stake. Scientists have vested interests and don't 
want to admit that they're wrong.

I'm not saying that I necessarily believe this hypothesis, but it does 
adequately explain the data available and I believe it warrants further 
investigation - I can't see NIH or anyone like that agreeing though, so such 
research will probably never get funded.

What do other people think?

Richard Burge         | e-mail:
King's College London |  R.Burge at bay.cc.kcl.ac.uk

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