PMC:7463108 / 76920-80606 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":"Host Genetics\nHost genetic variability can be a major determinant in individual susceptibility to HIV infectivity and may influence neuroHIV progression in the context of opiate co-exposure. The importance of CCR5 for HIV infectivity and polymorphisms in this gene are well established. Individuals who are homozygous in the CCR5 gene (CCR5Δ32) are highly resistant to infection by CCR5- (R5-) tropic HIV as demonstrated by individuals heterozygous for CCR5Δ32 who display partial resistance to infection and slower disease progression (Huang et al. 1996; Liu et al. 1996; van Rij et al. 1999). Besides CCR5, polymorphisms of other chemokine co-receptors and/or their cognate ligands have been implicated in HIV infectivity, including CCR2 (Smith et al. 1997; Kostrikis et al. 1998), CCL5 (Liu et al. 1999; McDermott et al. 2000), and CXCL12 (Winkler et al. 1998). Authoritative reviews on other gene polymorphisms that modify HIV infectivity and disease progression have been published (Lama and Planelles 2007; Singh and Spector 2009; Chatterjee 2010; Aouizerat et al. 2011).\nGene 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 HIV-1.\nNineteen different OPRM1 spliced variants have been described in humans (Pasternak 2004, 2014; Xu et al. 2014a; Lu et al. 2015). OPRM1 alternative splicing may also influence susceptibility to HIV-1 infection (Dever et al. 2012, 2014). Although many variants are thought to be non-functional and fail to traffic from the endoplasmic reticulum, increasing evidence suggests they may oligomerize other G Protein-coupled receptors or bind chaperones to assist in trafficking to the plasma membrane (Samoshkin et al. 2015; Zhu et al. 2019). Quantitative and qualitative differences in human MOR splice variant expression levels have been noted across different CNS cell types following exposure to HIV (Dever et al. 2012, 2014). Interestingly, an excitatory, MOR-1 K splice variant, that couples to GαS (Gris et al. 2010) is preferentially expressed in human astroglia (Dever et al. 2012) and has been shown to correlate with HIVE and cognitive impairment (Dever et al. 2012, 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