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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.1105642

Received for publication November 9, 2005.
Revised February 14, 2006.
Accepted for publication February 16, 2006.

Article

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 *@

*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

@ To whom correspondence should be addressed. E-mail: ho{at}email.chop.edu.


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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 {beta}-endorphin production and induced µ-opioid receptor mRNA expression in PBL and CEMX174 cells. The role of {beta}-endorphin in alcohol-mediated enhancement of HIV infection was indicated by the observations that naltrexone and CTAP antagonized ether alcohol- or exogenous {beta}-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: {beta}-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
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