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Enhancement of HIV-1 Replication by Opiates and Cocaine: The Cytokine Connection

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Drugs of Abuse, Immunity, and AIDS

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 335))

Abstract

In recent years, drug abuse has been identified as the most important factor in the spread of the AIDS epidemic (1). In the injection drug use (IDU) population, the sharing of contaminated injection equipment is a major means of transmitting HIV-1 (2, 3), the primary etiologic agent of AIDS. Several reports suggest that the course of HIV-1 infection is accelerated and that the mortality is increased in IDU patients (4–7), although results of some studies are contradictory (8, 9). As in other AIDS risk groups, multiple co-factors have been considered as possible contributors to the development of AIDS in HIV-1-infected drug abusers (10). A special cofactor postulated to be important in this patient group has been drug-induced immunologic disturbances (11, 12). This “co-factor hypothesis” is supported by a large body of evidence from clinical studies, animal models, and in vitro investigations (reviewed in 13–19).

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Authors and Affiliations

  1. Department of Medicine, Hennepin County Medical Center, USA

    Phillip K. Peterson, Genya Gekker, Ronald Schut, Shuxian Hu, Henry H. Balfour Jr. & Chun C. Chao

  2. Department of Laboratory Medicine and Pathology, University of Minnesota Health Sciences Center, University of Minnesota Medical School, Minneapolis, MN, USA

    Phillip K. Peterson, Genya Gekker, Ronald Schut, Shuxian Hu, Henry H. Balfour Jr. & Chun C. Chao

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  1. Phillip K. Peterson
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  1. University of South Florida, Tampa, Florida, USA

    Herman Friedman , Thomas W. Klein  & Steven Specter ,  & 

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Peterson, P.K., Gekker, G., Schut, R., Hu, S., Balfour, H.H., Chao, C.C. (1993). Enhancement of HIV-1 Replication by Opiates and Cocaine: The Cytokine Connection. In: Friedman, H., Klein, T.W., Specter, S. (eds) Drugs of Abuse, Immunity, and AIDS. Advances in Experimental Medicine and Biology, vol 335. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2980-4_26

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  • DOI: https://doi.org/10.1007/978-1-4615-2980-4_26

  • Publisher Name: Springer, Boston, MA

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