The AIDS epidemic in Africa is very different from the epidemic in the West. As suggested here by Zvi Bentwich, Alexander Kalinkovich and Ziva Weisman, this appears to be primarily a consequence of the over-activation of the immune system in the African population, owing to the extremely high prevalence of infections, particularly helminthic, in Africa. Such activation shifts the cytokine balance towards a T helper 0/2 (Th0/2)-type response, which makes the host more susceptible to infection with human immunodeficiency virus (HIV) and less able to cope with it.
PIP: The AIDS epidemic in Africa is very different from the epidemic in the West. Specifically, the following features of the AIDS epidemic in Africa distinguish it from the pattern of AIDS in North America and Europe: it is mainly a heterosexually transmitted disease with a male:female ratio of 1:1, and lacks the male homosexual and IV drug user risk groups; it is probably transmitted more easily; the progression of infection and disease is faster; and the clinical manifestations are different. This pattern of epidemic is also rapidly unfolding in Thailand, India, South America, and the Caribbean. Common to all regions in which this pattern dominates is the important role of prostitutes who comprise the major, initial reservoir of HIV from which it spreads into the general population as a sexually transmitted disease (STD). This pattern of spread has not, however, been found in the West or in other developed countries such as Japan, Australia, or New Zealand, where the prevalence of HIV infection among prostitutes remains low and is mostly associated with IV drug use. The widespread prevalence of STDs, the practice of scarification, transfusion, and the state of hygiene and nutrition in Africa may facilitate the transmission of HIV. The authors hypothesize, however, that the AIDS epidemics in the West and Africa are so different from each other because of a widespread altered background immune response among Africans. Infections, especially helminth infections, are endemic in Africa. Frequent exposure to these infections causes individual immune systems to be activated, or activated, thereby shifting the cytokine balance in such a manner which makes the host more susceptible to infection with HIV and less able to cope with it. Specifically, exposure to endemic infections has caused a shift away from an initial T1 helper cell response which would occur in the uninfected person to a less protective T helper 0/2-type response. Other types of immune activation have also taken place in the African population. This altered background immune response must be considered when designing vaccines and developing new therapies for HIV in Africa and other developing countries.