Morphine effects on HTLV-I infection in the presence or absence of concurrent HIV-1 infection.

Important note: Information in this article was accurate in 1999. The state of the art may have changed since the publication date.

Morphine effects on HTLV-I infection in the presence or absence of concurrent HIV-1 infection.

DNA Cell Biol. 1999 Apr;18(4):285-91. Unique Identifier : AIDSLINE MED/99249190
Nyland SB; Specter S; Ugen KE; Department of Medical Microbiology and Immunology, University of; South Florida College of Medicine, Tampa 33612, USA.

Abstract: Human T-cell leukemia virus type I (HTLV-I) infection is emerging as an important complication in HIV infection and AIDS in injecting drug users. HIV-1 and HTLV-I share a common host in CD4+ T lymphocytes. However, the result of HIV-1 infection is the decimation of this cell population, whereas a hallmark of HTLV-I infection is the inappropriate proliferation of infected cells. Combined epidemiologic data suggest that HTLV-I infection is enhanced during concurrent HIV-1/HTLV-I infection; however, there are currently no in vitro studies focusing on the effects of drugs of abuse on retrovirus coinfection. We have found that in an in vitro coinfection system (HIV-1 + HTLV-I), morphine treatment further enhanced the levels of HTLV-I p19. In addition, indicators of in vitro infection by cell-free HIV-1 were reduced by morphine treatment in both single and dual in vitro infection experiments. Interleukin 2 levels in the affected cultures were found to increase with combined HTLV-I infection and morphine treatment. These in vitro results indicate the need to further explore the activity of HTLV-I within opiate-treated cells, as this oncoretrovirus appears to be especially sensitive to morphine-induced alterations to its host cell environment.

Keywords: JOURNAL ARTICLE Cell Line Cytopathogenic Effect, Viral Gene Products, gag/BIOSYNTHESIS Human HIV-1/*DRUG EFFECTS/PHYSIOLOGY HTLV-I/*DRUG EFFECTS/PHYSIOLOGY Interleukin-2/BIOSYNTHESIS Morphine/*PHARMACOLOGY Retroviridae Proteins, Oncogenic/BIOSYNTHESIS Support, U.S. Gov't, P.H.S.
990830
A9981021

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