|Turned up to eleven: Fair and Balanced|
Thursday, April 04, 2002
Charles Murtaugh has a bunch of interesting biomedical science articles on his site, and one on HIV/AIDS in Africa in particular that I would like to elaborate on. Here is a quote;
Lowe poses, but doesn't answer, the question of why sub-Saharan Africa has such endemic HIV infection. In the U.S., as Michael Fumento has extensively documented (see, I told you I usually agree with Fumento), HIV has still made few inroads into the heterosexual population, excepting IV drug users. It seems hard to imagine that there are a lot more gays or IV drug users in Africa, so there must be some other reason explaining the rapid spread of HIV there.
I am inclined to disagree with Charles here, although social factors surely play a role, and may turn out to be the most important in the spread of HIV in Africa, there is an additional pathogenesis difference that has been completely unreported, to my knowledge, in the press. The details are complicated, and without a grounding in immunology, difficult to understand, but I will refer to my previous post on immunity(scroll down to March 20) for some of that. The adaptive immune system (T cells, B cells, located throughout the body, concentrated in lymph nodes and the spleen) is responsible, as I mentioned in that previous post, for response to specific pathogens. In particular, there is a complex system that determines, for a given infection, whether the body will choose to use humoral immunity (primarily antibodies) to defend itself, or cellular immunity (primarily cells which kill the invading cells, or host cells harboring a virus or intracellular bacterium). Infection with a virus, such as HIV, ought to stimulate the cellular immunity, which creates a specific type of T-cell called a Cytotoxic T-lymphocyte (CTL, often called a killer T-cell), which seeks out infected cells in the body, and kills them (this is in itself a very interesting process, but not our topic). Other infections, such as parasitic worm infections, cause induction of antibody responses primarily (this is sometimes called a Th2 response, because a type of T-cell called a T-helper 2 is formed that produces chemical signals that cause antibody production to be preferred to cytotoxic cell production). As always, there is some overlap in these systems, but the basic paradigm holds.
So, what does this have to do with HIV infection in Africa? In the developing world, parasitic infections are widespread. Among the most common are helminthic infections, and their staggering prevalence is described here. A lot of these infections are concentrated in sub-Saharan Africa (in particular, schistosomiasis, and trypanosomiasis(not a worm, but a parasite) are concentrated in these regions, but almost 1/2 of the world's population is infected with parasitic worms). It is not entirely clear what these infections may do in the context of HIV infection, but it is well known that parasitic worm infections drastically alter the immune responses in their hosts, and several reviews have posited a connection between disease course and parasitic co-infection. It has been suggested several times, in reputable scientific studies, that helminthic infections significantly alter the course of HIV disease (here is a review article abstract which makes a related claim for HIV and TB). I will note that this is a bit of a controversial idea, and research in a murine AIDS model suggests that it might be more complicated. I won't get into the problems with murine disease models, but I will note that sometimes, the comparisons are inapposite. There is also a possibility that infection may be affected, since the infection process for HIV is related to the presence of specific cell markers on the exterior of T-cells and macrophages, and the prevalence of those markers is directly related to the immune systems' choices of humoral v. cellular immunity. This possibility is backed up by epidemiological data. Because so called CD-4+ T-cells are the helper cells responsible for the choice, and they happen to be the target (or, more correctly, one of the targets) of HIV, it is clear that these coinfections are deeply intertwined, but the mechanisms and overall impacts are less clear. In effect, it may be that the prevalent helminthic infections and other parasites are priming the population specifically for HIV infections, or they make the disease manifest more quickly (this is almost certainly true), or both (as I think most likely).
This explanation, of course, is not great news for social conservatives, who would like to believe that promiscuity or other societal factors are to blame, and therefore the solution lies there. It's also not great news for liberal activists, who would like to cure AIDS by handing out condoms or by ending poverty (that last bit would certainly help, although I think clean water is much more important. In effect, though, the primary responsibility for curbing or curing HIV/AIDS must be in the scientific community, and the research, both primary and drug and vaccine development, is of paramount importance. Of course, as a working scientist, that makes me happy, so perhaps I am not a totally unbiased observer either (this gets pretty complex, huh?)