NIMH grantees Serena Spudich, M.D. , of Yale University, New Haven, Connecticut; Ronald Swanstrom, Ph.D. , of the University of North Carolina, Chapel Hill; Richard Price, M.D. , University of California, San Francisco; and Christa Buckheit Sturdevant, Ph.D., UNC (now at Duke), and colleagues, report on their findings March 26, 2015, in the journal PLoS Pathogens.
Prior to the study, it was known that HIV readily penetrates the brain and can trigger neurological problems and eventually cause dementia over the course of the infection. Yet there was little evidence about how quickly it can take hold and thrive there. Nor was it clear to what extent the brain serves as a hard-to-reach hideout from which the virus might re-infect the body – even if it is eliminated from peripheral blood and lymph node tissue by treatment.
To learn more, the researchers compared evidence of HIV activity in CSF versus blood from 72 untreated HIV-infected patients over the first two years of their infection. Overall, 10-22 percent of the patients showed evidence of HIV replication or inflammation in the brain at the different time points analyzed within the first two years – and the signs persisted over time in about 16 percent of the participants.
The evidence suggests that in most patients peripheral forms of the virus infect immune cells that spread to the brain via blood. Yet in some patients, genetic versions of the virus not found in blood evolve in the brain environment. So it could become an independent, compartmentalized viral reservoir, capable of generating treatment-resistant mutant forms that could break out and re-infect the rest of the body after seemingly successful treatment, explained Rausch.
Whether the potential brain damage caused by early HIV replication and inflammation might be reversible with antiviral therapy awaits further research, said Swanstrom.
Grants: MH099979, MH101024, MH094177, MH074466
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