Inflammatory processes have been suggested to underlie early neurologic abnormalities among persons living with HIV (HIV-positive), such as deficits in complex motor function, that are purported to remit with effective antiretroviral therapy (ART). We hypothesized that HIV will have negative direct and indirect effects through inflammation on complex motor performance.
The sample consisted of 90 ART-treated virally suppressed HIV-positive and 94 HIV-negative adults, aged 36–65 years, with balanced recruiting in each age decade (36–45, 46–55, and 56–65). Biomarkers of inflammation (d-dimer, IL-6, MCP-1/CCL2, sCD14, and TNF-α) were measured, and a composite inflammation burden score was calculated. Complex motor performance was evaluated using the Grooved Pegboard Test.
The HIV-positive group had worse complex motor performance (P = 0.001; Hedges g = −0.49) and a higher average inflammation burden composite score (P < 0.001; Hedges g = 0.78) than the HIV-negative group. Path analyses indicated that the indirect effect of HIV disease on complex motor performance through inflammation burden was statistically significant, accounting for 15.1% of the effect of HIV on complex motor performance.
Although neurologic findings (eg, deficits in motor speed/dexterity) commonly associated with HIV infection typically remit with ART, our analysis indicates that inflammation plays an important role in worse complex motor skills among HIV-positive adults. Future studies of strategies for managing chronic inflammation in HIV should consider using an inflammation burden composite and examining its effect on complex motor performance.
*Department of Psychiatry, University of California San Diego, San Diego, CA;
†SDSU/UCSD Joint Doctoral Program in Clinical Psychology, San Diego, CA;
‡Department of Neurosciences, University of California San Diego, San Diego, CA;
§Division of Infectious Diseases, School of Medicine, University of California San Diego, San Diego, CA; and
║Sam and Rose Stein Institute for Research on Aging, University of California San Diego, San Diego, CA.
Correspondence to: David J. Moore, PhD, HIV Neurobehavioral Research Program, 220 Dickinson Street, Suite B (8231), San Diego, CA 92103 (e-mail: email@example.com).
Supported by National Institute of Mental Health grant R01 MH099987 (multiple PI's: D.V.J. and D.J.M.). J.L.M., L.M.C., and E.W.P. were supported by NIDA T32 DA031098. The study was more broadly supported by the HIV Neurobehavioral Research Center (HNRC) Award P30MH062512 and NIH K24 MH097673 (PI: S.L.L.).
Presented at the annual Conference on Retroviruses and Opportunistic Infections (CROI); March 5, 2018; Boston, MA.
The authors have no funding or conflicts of interest to disclose.
Received June 16, 2018
Accepted August 10, 2018