HIV-I infection is characterized by a gradual loss of CD4(+) T cells and pr
ogressive immune deficiency that leads to opportunistic infections, otherwi
se rare malignancies and ultimately death. Extensive research over the past
two decades has increased our insight into the pathogenic mechanisms under
lying these features of HIV-I infection. Here, we will give a brief overvie
w of the most recent findings and present a model that fits most of the rel
evant aspects of HIV-I infection as known. We hypothesize that HIV-I infect
ion depletes T cell supplies (which are not replaced because of low and sta
tic thymic function) by direct infection and killing of cells and through h
yperactivation of the immune system.