CD8A and HIV infectious disease: Why are senescent, terminally differentiated and activated T cells, particularly CD8+ T cells, associated with comorbidities in the elderly and with accelerated epigenetic aging in HIV infection? Are they causative, contributory, or only correlative? Would senolytics change this landscape in the presence or absence of HIV?Is inflammation the major driving force behind the accelerated epigenetic aging observed in PWH, and if so, what underlying mechanism(s) elicits these changes?