Early treatment to halt neurological damage

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Soon after an individual’s initial infection with HIV, damage to brain volume and cortical thickness progressively worsens until anti-retroviral treatment is started, a study shows. “We knew HIV could cause neurological damage, but we did not know it happened so early in the infection,” said Serena Spudich, professor of neurology at Yale University and co-senior author of the paper. “The findings emphasise the importance of identifying infected people early and treating them so we can halt its progression.”

Scientists at the Montreal Neurological Institute and Hospital of McGill University analysed MRI data from 65 HIV-positive patients who had been longitudinally studied by Spudich. Their analysis found that the longer duration of infection before anti-retroviral treatment, the more damage was found in a variety of brain areas.

An estimated 36.7m people live with the infection but less than half have access to combination anti-retroviral treatment, which has extended the lifespan of millions of HIV patients.

Longer delays in treatment led to greater volume loss in the thalamus, caudate, and cerebellum, and to greater the cortical thinning in the frontal and temporal lobes, and cingulate cortex. Once combination retroviral treatment began, the volume changes in these regions stopped, and cortical thickness increased slightly in the frontal and temporal lobe, the study found.

Abstract
Background: HIV penetrates the brain in early infection. We used neuroimaging to longitudinally examine the impact of HIV and combination antiretroviral therapy (cART) on the brain in treated and untreated HIV-positive participants starting in primary HIV infection (PHI).
Methods: Sixty-five participants, enrolled during PHI, underwent longitudinal MRI, 30 of whom commenced cART during follow-up. Cross-sectional data from 16 chronic HIV-infected (CHI) and 19 HIV-negative participants were included for comparison. Brain volume and cortical thickness was estimated using tensor-based morphometry (TBM) and cortical modeling, respectively. Mixed-effects models longitudinally mapped structural brain changes before and after cART initiation. The relationship between brain morphometry estimates and blood and CSF biomarkers were also tested. Region-of-interest analyses were performed cross-sectionally to compare brain volume and cortical thickness between the groups.
Results: Prior to cART initiation, longer duration of untreated infection in PHI correlated with volume loss in the thalamus, caudate, and cerebellum, and with cortical thinning in the frontal and temporal lobes, and cingulate cortex. After cART, no further volume loss was observed. However, small increases of cortical thickness in the frontal and temporal lobe correlated with longer cART duration. No correlations were observed with blood or CSF measures. The PHI group did not have different brain volume or cortical thickness measures compared to the HIV-negative group, but had larger volumes in the thalamus, caudate, putamen, brainstem, and cortical gray matter compared with CHI participants.
Conclusion: Subcortical atrophy and cortical thinning occur during untreated infection but may be arrested by cART. These findings emphasize the importance of early cART.

Authors
Ryan Sanford Beau M Ances Dieter J Meyerhoff Richard W Price Dietmar Fuchs Henrik Zetterberg Serena Spudich D Louis Collins

Yale University material
Journal of Clinical Infectious Diseases abstract


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