PMC:7463108 / 52509-53331
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":"Glial-derived neuronal injury is not unidirectional. Neuronal damage-associated molecular patterns (DAMPs) and dysfunction can trigger both infected and uninfected glia to become reactive, resulting in further neuronal damage and escalating pathology. Neuronal injury can reactivate HIV in latently infected microglia (Alvarez-Carbonell et al. 2019). While the events underlying the disruption of neuronal-microglial activation that trigger the emergence of latent HIV are unclear, the induction of HIV expression appears to involve the production of DAMPs by injured neurons and can be turned “on”, e.g., by methamphetamine-induced sigma-1 (σ1) receptor activation, TNF-α and IL-1β, and TLR3 activation can be turned “off” by CX3CL1/fractalkine or glucocorticoid receptor activation (Alvarez-Carbonell et al. 2017, 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