We studied early effects of Human Immunodeficiency Virus (HIV) on HIV associated neurocognitive disorder (HAND) and regional cerebral oxygen metabolism (rCMRO2).

Treatment-naive PLHIV underwent neurocognitive assessment and magnetic resonance (MR) measurement of rCMRO2 in white matter (WM) and lentiform nuclei(LN) with repeat after 12 months of ART. Age-, gender-, and race-matched controls underwent single MR measurements. The primary analyses compared rCMRO2 in WM and LN at 12 months among controls, PLHIV with and without symptomatic HAND. Secondary analyses compared rCMRO2 in WM and LN at baseline and 12 months in PLHIV with and without HAND worsening.

47 controls completed MR. 29 PLHIV completed baseline and 12-month assessments of HAND and rCMRO2. At baseline, 13% had no cognitive impairment (NO), 27% had Asymptomatic Neurocognitive Impairment (ANI), 60% had Mild Neurocognitive Disorder (MND), and none had HIV-associated dementia (HAD). At 12 months, 13% had NO, 20% had ANI, 50% had MND, and 17% had HAD). There were no statistically significant differences in rCMRO2 in WM and LN among controls and PLHIV with (MND+HAD) and without symptomatic HAND at 12 months (p > 0.025). In those without HAND worsening (N=21) rCMRO2 remained stable between baseline and 12-months. In those with HAND worsening (N=8) rCMRO2 measurement (ml/100g/min) showed a downward trend from baseline to 12-months in WM (2.05±0.40 to 1.73±0.51, p=0.03) and LN (4.32±0.39 to 4.00±0.51, p=0.05).

In early stages of HIV, we found no association between cognitive dysfunction  and rCMRO2 in subcortical WM and LN even though symptomatic cognitive impairment  was noted in the majority of treatment-naïve participants, with worsening at 12 months despite ART. rCMRO2 may be a biomarker of cognitive decline in PLHIV, but will require further study.