Immunopathogenic mechanisms of HIV infection.
The acquired immunodeficiency syndrome (AIDS) follows infection with the human immunodeficiency virus (HIV) after a long and variable period of time. Although HIV can be rapidly cytopathic in vitro for T4 cells, during early in vivo infection, T4 cell numbers are normal and few infected T4 cells can be found. There is increasing evidence that cells of the monocyte/macrophage lineage, including bone marrow precursor cells, can be infected by HIV and are relatively resistant to the cytopathic effects of the virus. As in other lentivirus infections, the monocyte/macrophage may serve as a reservoir of HIV in the body and may play a major role in the pathogenesis of AIDS. In vitro induction of HIV from a latent or low level chronic infection to an active state results from exposure to physiologic cellular inductive signals that might be encountered during normal immune responses.
Rosenberg
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National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892.
Fauci
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AS
D000163:Acquired Immunodeficiency Syndrome / Q000209:etiology / Q000276:immunology*; D001853:Bone Marrow / Q000382:microbiology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000382:microbiology; D002459:Cell Fusion; D003588:Cytopathogenic Effect, Viral; D006678:HIV / Q000472:pathogenicity* / Q000502:physiology; D006801:Humans; D008264:Macrophages / Q000382:microbiology; D009000:Monocytes / Q000382:microbiology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D014775:Virus Activation / Q000187:drug effects; D014779:Virus Replication / Q000187:drug effects
D014409:Tumor Necrosis Factor-alpha