PMC:7463108 / 63836-65154 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 likely damages OLs through both direct and indirect actions. OLs lack CD4, and reports of OL infection by HIV are variable (Esiri et al. 1991; Albright et al. 1996; Wohlschlaeger et al. 2009); thus, HIV infection of OLs is unlikely a major avenue of OL or white matter damage (discussed below). Alternatively, bystander damage to OLs through the production of “virotoxins” and “cellular toxins” (Nath 1999) by infected neighboring cells is more likely to be operative (Hauser et al. 2009; Zou et al. 2015; Jensen et al. 2019; Zou et al. 2019). ARVs also contribute to OL cytotoxicity (Jensen et al. 2015; Festa et al. 2019; Jensen et al. 2019). HIV-1 Tat directly induces damage in isolated OLs through α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/N-methyl-D-aspartic acid (NMDA) receptor-dependent mechanisms (Zou et al. 2015) and is also associated with abnormal Kv1.3 activity (Liu et al. 2017). Immature OLs are preferentially targeted by Tat compared to differentiated OLs (Khurdayan et al. 2004; Hahn et al. 2012; Zou et al. 2015, 2019). While the reasons why immature OLs are more susceptible to Tat are unclear, unlike mature OLs, Tat preferentially upregulates GSK-3β signaling in undifferentiated OLs by inhibiting Ca2+/calmodulin-dependent protein kinase II β (CaMKIIβ) (Zou et al. 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