Antiviral treatment normalizes neurophysiological but not movement abnormalities in simian immunodeficiency virus-infected monkeys

Simian immunodeficiency virus (SIV) infection of rhesus monkeys provides an excellent model of the central nervous system (CNS) consequences of HIV in fection. To discern the relationship between viral load and abnormalities i nduced in the CNS by the virus, we infected animals with SIV and later inst ituted antiviral treatment to lower peripheral viral load. Measurement of s ensory-evoked potentials, assessing CNS neuronal circuitry, revealed delaye d latencies after infection that could be reversed by lowering viral load. Cessation of treatment led to the reappearance of these abnormalities. In c ontrast, the decline in general motor activity induced by SN infection was unaffected by antiviral treatment. An acute increase in the level of the ch emokine monocyte chemoattractant protein-1 (MCP-1) was found in the cerebro spinal fluid (CSF) relative to plasma in the infected animals at the peak o f acute viremia, Likely contributing to an early influx of immune cells int o the CNS. Examination of the brains of the infected animals after return o f the electrophysiological abnormalities revealed diverse viral and inflamm atory findings. Although some of the physiological abnormalities resulting from SIV infection can be at least temporarily reversed by lowering viral l oad, the viral-host interactions initiated by infection may result in long- lasting changes in CNS-mediated functions.