Virologic and immunologic aspects of acquired immunodeficiency syndrome.
From the initial clinical descriptions of the acquired immunodeficiency syndrome (AIDS) in 1981 to the present time, much has been discovered concerning the epidemiologic factors, pathogenesis, treatment and prevention of this disease. Recent advances in epidemiology have included a better understanding of the occupational risk of human immunodeficiency virus (HIV) infection after percutaneous exposure (responsible for approximately 0.4 per cent of instances), an appreciation of the potential variability in the time interval between infection and seroconversion (generally on the order of three months but occasionally longer) and establishment of the need for intimate contact to transmit infection. Following the discovery of HIV-1 as the etiologic agent of AIDS, many rapid advances have been possible including the development of screening tests, elucidation of the HIV-1 genome and the discovery that the CD4 T lymphocyte is the predominant cell destroyed by HIV-1. Progressive destruction of CD4 T cells results in a progressive decline in immunologic function that may take a variety of clinical forms, ranging from no symptoms to severe opportunistic infections. The delineation of the life cycle of HIV-1 has helped in the development of antiretroviral therapies, including agents that interfere with reverse transcription (nucleoside analogues, such as zidovudine, dideoxycytidine, dideoxyinosine and azidodideoxyuridine) and agents that interfere with viral assembly (protease inhibitors and interferon alpha). A more precise understanding of the nature of the immune response elicited after HIV-1 infection has resulted in the development of several candidate HIV-1 vaccines, including recombinant vaccinia viruses expressing the HIV-1 envelope and recombinant envelope proteins.
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Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda 20892.
D000163:Acquired Immunodeficiency Syndrome / Q000097:blood / Q000276:immunology / Q000382:microbiology*; D015496:CD4-Positive T-Lymphocytes / Q000737:chemistry / Q000276:immunology / Q000502:physiology; D015497:HIV-1 / Q000254:growth & development* / Q000276:immunology / Q000472:pathogenicity; D006801:Humans