Neurologic complications of HIV disease and their treatment

Important new information regarding neurologic complications of HIV disease was presented at the 2007 Conference on Retroviruses and Opportunistic Infections. In addition to presentations on pathogenesis and treatment of neurologic complications, the conference included findings that have implications for the management of HIV disease outside the nervous system. Key findings included that the distribution of antiretrovirals into the central nervous system may influence the effectiveness of treatment outside this protected compartment; that postponing initiation of therapy until blood CD4+ counts fall to 300 cells/mm3 may increase the risk for HIV-associated neurocognitive impairment but interruption of antiretroviral therapy in individuals with high CD4+ counts may have neuropsychologic benefits; that substantial changes, including macrophage activation and neuronal injury can occur shortly after HIV transmission; that HIV can influence neural progenitor cells to decrease neuronal differentiation; that newer neuroimaging technologies, such as diffusion tensor imaging and blood oxygen level-dependent functional magnetic resonance imaging can identify important effects of HIV on the brain such as alterations in cerebral oxygen consumption; that serotonin reuptake inhibitors and 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors may reduce HIV RNA levels in cerebral spinal fluid; and that erythropoietin and the non-immunosuppressive immunophilin ligand, GPI-1046, may improve HIV-associated injury of peripheral nerves. The conference also included an important focus on JC virus encephalitis (also known as progressive multifocal leukoencephalopathy).