Immunological features of human immunodeficiency virus disease

Infection with the human immunodeficiency viruses results in a profound immunosuppression responsible for most of the clinical features of AIDS. The virus devastates the immune system because its main target is the T4 lymphocyte, which is the key component for generating and regulating the immune response. The cellular receptor for HIV, the membrane glycoprotein CD4, is found mainly on the surface of this major subpopulation of T lymphocytes and also on many other cell types such as those of the monocyte/macrophage series. HIV can destroy CD4 cells by direct virus cytotoxicity and indirectly through the host response against HIV-infected cells or gp120-targeted cells. Cells of the macrophage lineage are generally not destroyed but serve as a reservoir of virus. HIV also causes functional impairment in T cells, B cells and monocytes. The virus can exist in latent or chronic form. The mechanisms of cellular destruction, viral persistence and conversion to a productive infection are being studied vigorously. Host factors that may affect clinical outcome and immunological markers that may predict progression of HIV disease are presently delineated. Prolonged serological latency may follow infection with HIV. Protective humoral and cell-mediated immune responses to HIV are either poor or not sustained. Recent results on HIV-specific cytotoxic T lymphocytes are of great interest. These cytotoxic cells, particularly those directed to gp120 targets, probably contribute to cellular damage. A central question regarding immunity to HIV is its beneficial versus deleterious effects, particularly in regard to the eventual development of an AIDS vaccine.