MAXIME SELIGMANN, M.D.; ANTHONY J. PINCHING, M.D.; FRED S. ROSEN, M.D.; JOHN L. FAHEY, M.D.; RAKHIM M. KHAITOV, M.D.; DAVID KLATZMANN, M.D.; SCOTT KOENIG, M.D.; NKANDU LUO, M.D.; JACOB NGU, M.D.; GERT RIETHMÜLLER, M.D.; THOMAS J. SPIRA, M.D.
Recent advances in the understanding of the pathogenesis of infection with human immunodeficiency virus (HIV) stems from the demonstration that the membrane glycoprotein, CD4, is the cellular receptor for HIV. This glycoprotein is found mainly on the surface of a major subpopulation of T lymphocytes and also on macrophages, natural killer cells, some B lymphocytes, and neuronal cells. Cells infected with HIV may be destroyed or have their normal function impaired. Host immune responses to HIV are poor and are not sustained. Neutralizing antibody often is not produced, or HIV may escape from normal immunosuppressive mechanisms through the process of rapid antigenic variation. Factors and markers that may be important in the outcome or that may predict progression of HIV infection are genetic (Gc type), environmental (nutritional status or intercurrent sexually transmitted diseases sustained by the host), and immunologic (rate of decline in number and impairment of function of CD4 + lymphocytes and of decline in antibody titers to HIV core protein, p24). A recombinant vaccine will probably be developed for testing in future clinical trials.
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SELIGMANN M, PINCHING AJ, ROSEN FS, FAHEY JL, KHAITOV RM, KLATZMANN D, et al. Immunology of Human Immunodeficiency Virus Infection and the Acquired Immunodeficiency Syndrome: An Update. Ann Intern Med. 1987;107:234–242. doi: 10.7326/0003-4819-107-2-234
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Published: Ann Intern Med. 1987;107(2):234-242.
HIV, Infectious Disease.
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