WASHINGTON: Researchers have discovered that HIV can begin replicating in the brain as early as four months after initial infection. An analysis of cerebral spinal fluid (CSF), a window into brain chemical activity, showed that for a subset of patients HIV had started replicating within the brain within the first four months of infection. CSF in 30 per cent of HIV-infected patients tracked showed at least transient signs of inflammation – suggesting an active infectious process – or viral replication within the first two years of infection.

There was also evidence that the mutating virus can evolve a genome in the central nervous system that is distinct from that in the periphery. “These results underscore the importance of early diagnosis and treatment with antiretroviral therapy,” said Dianne Rausch, director of the Division of AIDS Research of the NIH’s National Institute of Mental Health (NIMH) in the US.

“Any delay runs the risk that the virus could find refuge and cause damage in the brain, where some medications are less effective – potentially enabling it to re-emerge, even after it is suppressed in the periphery,” Rausch said. 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 per cent of the patients showed evidence of HIV replication or inflammation in the brain at the different time points analysed within the first two years – and the signs persisted over time in about 16 per cent 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, compartmentalised 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, said Rausch.

Whether the potential brain damage caused by early HIV replication and inflammation might be reversible with antiviral therapy awaits further research, researchers said. The study is published in the journal PLoS Pathogens.

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