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Originally published online as doi:10.1189/jlb.1105642 on March 30, 2006

Published online before print March 30, 2006
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(Journal of Leukocyte Biology. 2006;79:1166-1172.)
© 2006 by Society for Leukocyte Biology

Naltrexone inhibits alcohol-mediated enhancement of HIV infection of T lymphocytes

Xu Wang*, Steven D. Douglas*, Jin-Song Peng{dagger}, David S. Metzger{ddagger}, Charles P. O’Brien{ddagger}, Ting Zhang* and Wen-Zhe Ho*,1

* Division of Allergy and Immunology, Joseph Stokes Jr. Research Institute at the Children’s Hospital of Philadelphia, Department of Pediatrics, and
{ddagger} Department of Psychiatry, The Center for Studies of Addiction, University of Pennsylvania School of Medicine, Philadelphia; and
{dagger} Virology Laboratory, Wuhan Center for Disease Prevention and Control, People’s Republic of China

1Correspondence: Division of Allergy and Immunology, The Children’s Hospital of Philadelphia, 34th Street & Civic Center Boulevard, Philadelphia, PA 19104. E-mail: ho{at}email.chop.edu

ABSTRACT

Acute and chronic alcohol abuse impairs various functions of the immune system and thus, has been implicated as a cofactor in the immunopathogenesis of human immunodeficiency virus (HIV) disease progression. We determined whether naltrexone, an opioid receptor antagonist widely used in the treatment of alcoholism, inhibits alcohol-mediated enhancement of HIV infection of T cells. Alcohol enhanced HIV infection of peripheral blood lymphocytes (PBL) and a human lymphoid cell line (CEMX174). Alcohol increased HIV X4 envelope (Env), not murine leukemia virus Env-pseudotyped infection of CEMX174 cells. Naltrexone antagonized the enhancing effect of alcohol on HIV infection of PBL and CEMX174 cells. The specific µ-opioid receptor antagonist, Cys2, Tyr3, Arg5, Pen7 (CTAP) amide, also blocked the enhancing effect of alcohol on HIV infection. Investigation of the underlying mechanism for the alcohol action showed that alcohol significantly increased endogenous ß-endorphin production and induced µ-opioid receptor mRNA expression in PBL and CEMX174 cells. The role of ß-endorphin in alcohol-mediated enhancement of HIV infection was indicated by the observations that naltrexone and CTAP antagonized ether alcohol- or exogenous ß-endorphin-mediated enhancement of HIV infection. These findings suggest a biological mechanism for the potential therapeutic benefit of naltrexone in treating HIV-infected alcoholics.

Key Words: ß-endorphin • PBL • µ-opioid receptor • CTAP




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X. Wang, S. D. Douglas, J.-S. Peng, D.-J. Zhou, Q. Wan, and W.-Z. Ho
An in Vitro Model of Morphine Withdrawal Manifests the Enhancing Effect on Human Immunodeficiency Virus Infection of Human T Lymphocytes through the Induction of Substance P
Am. J. Pathol., November 1, 2006; 169(5): 1663 - 1670.
[Abstract] [Full Text] [PDF]


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