Christine M. Hogan, MD; Scott M. Hammer, MD
Part 2 of this review will appear in the 15 May 2001 issue.
Acknowledgment: The authors thank Brian-Fred Fitzsimmons, MD, for assistance with preparation of the figures.
Grant Support: Dr. Hammer is supported by grants AI46386 and AI48013 from the National Institute of Allergy and Infectious Diseases. Dr. Hogan is supported in part by Center for AIDS Research grant 5P30AI42848-03 from the National Institute of Health and the National Institute of Allergy and Infectious Diseases, and in part by the SmithKline Beecham Development Partners Junior Faculty Award.
Requests for Single Reprints: Christine M. Hogan, MD, Columbia University, College of Physicians and Surgeons, Division of Infectious Diseases, P & S Box 82, 630 West 168th Street, New York, NY 10032; e-mail, firstname.lastname@example.org.
Current Author Addresses: Drs. Hogan and Hammer: Columbia University, College of Physicians and Surgeons, Division of Infectious Diseases, P & S Box 82, 630 West 168th Street, New York, NY 10032.
The course of HIV infection varies widely among individuals. Long-term nonprogressors or slow progressors may remain asymptomatic and have normal CD4 counts despite more than a decade of untreated HIV infection. In contrast, rapid progressors develop AIDS within 5 years. In addition, some persons remain uninfected despite repeated exposure to HIV. Immunologic and genetic studies of long-term nonprogressors and exposed yet uninfected persons, as well as data from studies of primary HIV infection, have helped to elucidate the mechanisms by which some persons are protected from HIV acquisition or have slow rates of disease progression. This review (the first of two parts) describes what is currently known about host factors in HIV-1 infection. Studies for inclusion were identified by a systematic search of PubMed for English-language literature published from 1988 through June 2000. Abstracts of presentations at major meetings convened in 2000 were also included if appropriate. Growing evidence suggests a crucial role of cytotoxic T cells and T-helper cells in controlling viremia, slowing disease progression, and perhaps preventing establishment of infection. Humoral and mucosal immunity, soluble inhibitory factors, the cytokine milieu, and concomitant infections also affect outcome. Genetic host factors, such as inheritance of mutant chemokine receptors or certain HLA types, affect susceptibility to infection and subsequent clinical course. The role of cellular and humoral immunity, mucosal immunity, and other local factors in determining the course of HIV infection is discussed.
Hogan CM, Hammer SM. Host Determinants in HIV Infection and Disease: Part 1: Cellular and Humoral Immune Responses*. Ann Intern Med. 2001;134:761–776. doi: 10.7326/0003-4819-134-9_Part_1-200105010-00013
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Published: Ann Intern Med. 2001;134(9_Part_1):761-776.
HIV, Infectious Disease.
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