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Immunopathogenic Mechanisms in Human Immunodeficiency Virus (HIV) Infection

Anthony S. Fauci, MD; Steven M. Schnittman, MD; Guido Poli, MD; Scott Koenig, MD; and Giuseppe Pantaleo, MD
[+] Article and Author Information

Requests for Reprints: Anthony S. Fauci, MD, National Institute of Allergy and Infectious Diseases, Building 31, Room 7A03, 9000 Rockville Pike, Bethesda, MD 20892.

Current Author Addresses: Dr. Fauci: National Institute of Allergy and Infectious Diseases, Building 31, Room 7A03, 9000 Rockville Pike, Bethesda, MD 20892.

Drs. Schnittman, PoIi, Koenig, and Pantaleo: Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, Building 10, Room 11B-13, 9000 Rockville Pike, Bethesda, MD 20892.


Ann Intern Med. 1991;114(8):678-693. doi:10.7326/0003-4819-114-8-678
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An understanding of the immunopathogenic mechanisms of infection with human immunodeficiency virus (HIV) is fundamental in developing successful approaches to designing effective therapeutic and vaccine strategies. In this regard, we have investigated the mechanisms by which HIV inserts itself into the human immune system and uses the elaborate cytokine network to its own replicative advantage. We have also shown that the burden of HIV in CD4+ T cells is directly associated with a decline in this cell population in vivo and a progression to disease. Mononuclear phagocytes may play a role in the pathogenesis of HIV infection by serving as reservoirs of the virus. Of note is the fact that monocytes in the peripheral blood of HIV-infected individuals are rarely infected in vivo, whereas infected-tissue macrophages may play a role in organ-specific HIV-related pathogenesis. The role of HIV-specific humoral and cell-mediated immunity in HIV infection is not well understood. However, fine specificity of responses against HIV have been delineated in some in-vitro systems. It is unclear why these responses, particularly HIV-specific cytolytic T-cell responses, diminish over the course of infection and are unable to contain progression of infection.

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