Mitochondrial reactivity following acute exposure to experimental pain testing in people with HIV and chronic pain

Shannon R Gilstrap, Joanna M Hobson, Michael A Owens, Dyan M White, Melissa J Sammy, Scott Ballinger, Robert E Sorge, Burel R Goodin

Physical stressors can cause a physiological response that can contribute to an increase in mitochondrial dysfunction and mtDNA damage. People living with HIV (PWH) are more likely to suffer from chronic pain and may be more susceptible to mitochondrial dysfunction following exposure to a stressor. We used Quantitative Sensory Testing (QST) as an acute painful stressor in order to investigate whether PWH with/without chronic pain show differential mitochondrial physiological responses. The current study included PWH with (n=26), and without (n=29), chronic pain. Participants completed a single session that lasted approximately 180 minutes, including QST. Blood was taken prior to and following the QST battery for assays measuring mtDNA damage, mtDNA copy number, and mtDNA damage-associated molecular pattern (DAMP) levels (i.e. ND1 and ND6). We examined differences between those with and without pain on various indicators of mitochondrial reactivity following exposure to QST. However, only ND6 and mtDNA damage were shown to be statistically significant between pain groups. PWH with chronic pain showed greater mitochondrial reactivity to laboratory stressors. Consequently, PWH and chronic pain may be more susceptible to conditions in which mitochondrial damage/dysfunction play a central role, such as cognitive decline.