Apoptosis and HIV infection: T-cells fiddle while the immune system burns

Enhancement of programmed cell death (apoptosis) of CD4 T-cells by human immunodeficiency virus (HIV) is thought to be an important factor in the pathogenesis of HIV disease. Recent studies have cast doubt on this concept, however, portraying apoptosis as a potent antiviral strategy to eliminate infected cells. These studies have shed new light on the role of apoptosis in HIV infection. While cellular and immunologic mechanisms of apoptosis purge the HIV-infected lymphoid cell population, HIV thwarts apoptosis in myeloid cells, particularly monocyte/macrophages. Although HIV protease inhibitor therapy partially reverses the lymphoid cell process, this therapeutic approach fails to counter the persistence of HIV infection in myeloid cells. Thus apoptosis of T-cells may be a futile host attempt to control the spread of HIV while the infection smoulders in monocyte/macrophages. In other words, the antiviral defense system fiddles while the immune system burns.