Morphine induces gene expression of CCR5 in human CEM x174 lymphocytes

All HIV-1 strains studied to date use CCR5, CXCR4, or both receptors to ent er cells, Simian immunodeficiency virus (SIV) infection of non-human primat es has served as a useful model for understanding AIDS pathogenesis in huma ns. Research on several genetically divergent SIV isolates has revealed tha t SIV uses CCR5, and not CXCR4, for entry. CEMx174, a human lymphoid cell l ine, has been routinely used to cultivate and maintain various SIV strains, However, questions have arisen about how CEMx174, which reportedly was una ble to express detectable amounts of CCR5 transcripts, efficiently supports the growth of SIV. In searching for an answer, we resorted to a sensitive competitive reverse transcriptase-polymerase chain reaction procedure in an attempt to detect as well as quantify the amount of CCR5 expression. Here we present our findings, which indicate that CEMx174 indeed expresses CCR5 and that the amount of CCR5 is increased in cells pretreated with morphine. These results correlate well with our previous observations that morphine treatment causes CEMx174 cells to be more susceptible to SIV infection, Sim ilar morphine effect was not observed on CEMx174 cells infected with simian retroviruses, which do not depend on CCR5 for entry. These findings sugges t a plausible mechanism whereby opiate drug users render themselves more su sceptible to HIV infection, thereby explaining the vast prevalence of HIV i nfection among endemic drug use populations.