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(American Journal of Pathology. 2006;169:1663-1670.)
© 2006 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2006.060358

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

Xu Wang*{dagger}, Steven D. Douglas*, Jin-Song Peng{ddagger}, Dun-Jin Zhou{ddagger}, Qi Wan* and Wen-Zhe Ho*§

From the Department of Pediatrics,* Division of Allergy and Immunology, Joseph Stokes Jr. Research Institute at the Children’s Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania; the Virology Laboratory,{ddagger} Wuhan Center for Disease Prevention and Control, Wuhan, People’s Republic of China; the Department of Pediatrics,§ Renmin Hospital of Wuhan University, Wuhan, People’s Republic of China; and The College of Life Science,{dagger} Central China of Normal University, Wuhan, People’s Republic of China

Opioid withdrawal is a crucial and recurring event during the course of opioid abuse that has a negative impact on the immune system. In this study, we investigated whether abrupt withdrawal (AW) or precipitated withdrawal (PW) potentiates human immunodeficiency virus (HIV) infection of human T lymphocytes. AW and PW enhanced HIV infection of peripheral blood lymphocytes and T-cell lines (Jurkat and CEMX174). In addition, both AW and PW induced HIV replication in a latently HIV-infected human T-cell line (J1.1). The enhancing effect of AW and PW was associated with the induction of neuropeptide substance P in both peripheral blood lymphocytes and the T-cell lines. The substance P receptor antagonist, CP-96,345, not only blocked AW- or PW-induced endogenous substance P expression but also abrogated AW- or PW-induced HIV replication in T cells. These findings provide a cellular mechanism that supports the notion that opioids have a co-factor role in promoting HIV infection of the immune cells.






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Copyright © 2006 by the American Society for Investigative Pathology.