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Abstract: 

HIV can persist in the brain despite antiviral treatment, contributing to chronic inflammation, accelerated brain aging, and cognitive impairment. New research reveals that one seemingly promising strategy for reducing this inflammation may have the opposite effect. In animal studies, blocking the alpha-4 integrin to limit immune-cell entry into the brain unexpectedly increased viral levels by reducing protective killer T cells while allowing HIV-carrying helper T cells to remain. The findings illuminate the complex role of immune surveillance in controlling HIV within the central nervous system and suggest that future therapies must target immune cells more precisely to reduce neuroinflammation without weakening the brain’s defenses against the virus.

Keywords: HIV; Neuroinflammation; Central Nervous System; T Cells; Integrins; Neurodegeneration

Affiliations:  1: University of Virginia.