PMC:7463108 / 67505-68675
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7463108","sourcedb":"PMC","sourceid":"7463108","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7463108","text":"Even though neural progenitors (Krathwohl and Kaiser 2004; Lawrence et al. 2004; Rothenaigner et al. 2007; Schwartz et al. 2007; Balinang et al. 2017), neuroblast cell lines (Ensoli et al. 1994; Rothenaigner et al. 2007), and/or immature astroglia (Atwood et al. 1993; Tornatore et al. 1994; Barat et al. 2018) can harbor HIV infection (reviewed by Hauser and Knapp 2014; Putatunda et al. 2019), the degree to which they are a source of active infection or serve as a latent viral reservoir (Blankson et al. 2002; Bruner et al. 2019) by retaining intact proviral DNA within incipient macroglial progeny is uncertain. In fact, spurious reports of HIV-infected adult neurons (Torres-Munoz et al. 2001; Canto-Nogues et al. 2005) may result from the retention of proviral genes that integrated into pluripotent neural progenitors or neuroblasts at earlier stages during maturation. Importantly, prolonged exposure to opioids can increase the production of HIV in human neural progenitor cells (hNPCs). Exposure of R5-tropic HIVBaL-infected hNPCs to morphine continuously for 21 d increased viral production compared to HIVBaL infection alone in vitro (Balinang et al. 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