PMC:7463108 / 73539-76918 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":"HIV-1 Genetics\nGenetic differences among HIV-1 variants have a significant impact on HIV transmission, disease progression, as well as the response to ARV therapy (see reviews, Geretti 2006; Taylor et al. 2008; Tyor et al. 2013; Tables 1 and 2). Pre-cART studies provide substantial evidence that HIV clade differences can influence HAND (Gupta et al. 2007; Sacktor et al. 2009; Boivin et al. 2010; McArthur et al. 2010; Rao et al. 2013), with HAND severity being highest for clade D and B strains, followed by C and A clades (Tyor et al. 2013). These findings are supported by preclinical studies in which clade B or clade C HIV-infected macrophages were intracranially injected into severe combined immunodeficient mice (SCID) mice. Exposure to clade B isolates induced more severe memory deficits, as well as greater astrogliosis and neuronal damage (Rao et al. 2008, 2013). In another example, the Tat dicysteine motif (CC) at positions 30 and 31, which is commonly found in clade B isolates, appears to worsen HAND (Mishra et al. 2008; Rao et al. 2013) and has been studied extensively in vitro (Ranga et al. 2004; Rao et al. 2008; Zou et al. 2011; Krishnan and Chatterjee 2015). Clade B Tat is more intrinsically cytotoxic to primary neurons in vitro than clade C Tat (Li et al. 2008; Campbell et al. 2011; Zou et al. 2011), resulting in increased proinflammatory cytokine production (e.g., IL-6 and TNF-α) (Gandhi et al. 2009) and monocyte recruitment/migration into the brain (Ranga et al. 2004; Rao et al. 2008), and increased disruption of the BBB (Gandhi et al. 2010). Similarly, the production of the inflammatory mediators prostaglandin E2 and the thromboxane A2 receptor by astrocytes is more significantly increased by clade B than clade C gp120 (Samikkannu et al. 2011). Sequence and structural alterations in gp120 have been demonstrated between clades B and C (Gnanakaran et al. 2007) and potentially contribute to these observed differences.\nWhen considering effects of HIV clade variants in the presence of opioids, the overall toxicity in MSNs seen with clade C Tat (30% neuronal losses) was considerably less than with clade B (70% losses) (Zou et al. 2011). Although clade B HIV predominates in Western countries, future clinical longitudinal studies are necessary that employ HIV clade testing in HIV-1 infected opioid users to confirm the hypothesis that opioid interactive effects on HAND pathogenesis depend on the HIV clade assessed.\nBesides HIV genetic diversity, differences in HIV tropism add another level of complexity. Morphine interactions can differ significantly between X4 and R5-tropic gp120 variants depending on the outcome measure (El-Hage et al. 2011b; Podhaizer et al. 2012; Balinang et al. 2017; Kim et al. 2018). Increased infectivity in the presence of morphine was noted for the R5-tropic HIV-1SF162 strain in a human hepatoma Huh7.5.1 cell line model, whereas the infectivity rate with the X4-tropic HIV-1LAI/IIIB strain was unaffected by morphine (El-Hage et al. 2011b).\nTo date, no clinical studies have assessed whether opioid interactions with R5- or R4-preferring HIV strains differentially impact the severity of HAND. However, the findings from preclinical studies indicate that HIV-1 strain-specific differences are critical determinants in shaping both the timing and pattern of neurotoxic interactions with opioid 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