PMC:7463108 / 77998-79627 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7463108","sourcedb":"PMC","sourceid":"7463108","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7463108","text":"Gene polymorphisms of opioid (OPRM1 and OPRK1) and non-opioid (e.g., DRD1 and DRD2) drug/neurotransmitter receptor genes are associated with altered HIV infectivity, viral loads and CD4+ cell counts (Proudnikov et al. 2012; Regan et al. 2012; Jacobs et al. 2013; Proudnikov et al. 2013; Dever et al. 2014). Not only do MORs mediate the behavioral consequences of opiate abuse (Bond et al. 1998; Szeto et al. 2001; Ikeda et al. 2005; Kreek et al. 2005; Xu et al. 2014b), but the ability of MOR to modulate HIV chemokine co-receptor signaling through cross desensitization or through direct molecular interactions suggest MOR may influence HIV infectivity at multiple levels. The unique ability of MOR to modulate HIV co-receptor function, prompted inquiry regarding whether variants of the OPRM1 gene (polymorphisms or splicing variants) might differentially effect HIV infectivity and/or opiate addictive behaviors. In a sample of 1031 HIV-1-infected women, 18 OPRM1 polymorphisms were significantly associated with decreases or increases in HIV infectivity and responsiveness to cART (Proudnikov et al. 2012). Other gene polymorphisms, such as enzymes affecting drug metabolism (Meyer and Zanger 1997; Benowitz et al. 2006) and other neurochemical systems (Herman and Balogh 2012; Koob and Volkow 2016) can also affect drug dependence. The A118G variant of OPRM1 alters the regulation of proinflammatory cytokine secretion (i.e., TNF-α, IL-10, IFN-γ) from peripheral immune cells (Matsunaga et al. 2009). Overall, these findings suggest that polymorphisms in MOR ligands/genes (OPRM1) can influence the pathophysiology of 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