Viral Load levels of HIV and HHV-6A

[T.J. Fitzmaurice]

In article <3id4a7$4a2 at panix.com>, James Scutero <jscutero at panix.com> wrote:
>Actually there is a very high correlation between HHV-6 and AIDS if you 
>consider the fact that active infection with HHV-6 is twice that of CMV in
>people who have AIDS. Knox KK, Carrigan DR. Disseminated active HHV-6 
>infection in patients with AIDS. Lancet 1994;343:577-578.
>
>Researchers estimate that 80 to 90 percent of people are infected with 
>HHV-6 before they turn four years old. That is a very high correlation.
Two points on the above, one a point of logic, the other a point of 
science 
1) In a post a little further downstream in this thread, Mr Scutero,
you point in a review that goes on about how low incidence does not
preclude an agent being the infectious one, but you use incidence here
to remove CMV from the equation. It just appears to be arguing using both
sides of the fence.

2) EBV is ubiquitous, 90%+ of the population carry it. On correlation
it is a better option than HHV-6. BUT with such high incidences of the
virus, how can the low (over the entire population) incidence of 
full-blown AIDS be explained. As you are using high incidence of HHV-6
as evidence, this precludes IMHO the answer to this question, based on the
fact that low incidence does not mean the agent isn't the important one.
>
>>          2. How can this theory explain the fact that screening blood
>>          for HIV all but eliminates the spread of AIDS in blood
>>          products?
>>
>AIDS is not spread in the blood; HIV is spread in the blood. 
>AIDS is defined by immunosuppression plus HIV. If someone has 
>immune system suppression due to active HHV-6A infection, and he 
>does not have HIV, he is considered not to have AIDS.
>HHV-6 is not screened from the blood supply. Wilborn, F et al, Detection of
>herpesvirus type 6 by polymerase chain reaction in blood donors: random tests
>and prospective longitudinal studies. British Journal of Haematology, 1994,
>88, 187-192.
>
>-James M. Scutero
To phrase this better, How do you deal with the epidemiological evidence
that if you screen blood for HIV and remove it from circulation then
haemophiliac patients who develop HIV antibody and then become AIDS
sufferers are vastly reduced compared to before this occurence.

On the point of the herpesviruses, they are not like HIV. HIV is present
and active in the body for a long time. HHV 6 and other herpesviruses are
latent and thus bioogically inactive for most of the time. The CD4+
T-cell count would drop in fits and starts if HHV-6 was destroying them
as the virus went through phases of latency and reactivation, that became ever
more biased to reactivation. If a herpes virus were resposible for the
immunosuppression, it would have to be capable of doing more damge to th
circulating T-cells or their source than the body was capable of
regenerating befiore the next period of active virus growth (which could
be weeks/months or years), and this doesn't fit with what I know about
T-cell levels in HIV/AIDS (whatever dependant on each individuals belief).

Tim