Central nervous system abnormalities in pediatric human immunodeficiency virus infection

With the recent improvements in treatment of HIV, the disease has become a chronic one. The mean survival time of HIV-infected children is now 9-10 years, which is more than 4 times the mean age of such children who died in 1990. Yet, the prevalence of HIV encephalopathy has not decreased despite use of HAART. Rather, it is expected that as patients live longer, the prevalence of CNS manifestations will actually increase. Thus, more children can be expected to manifest encephalopathy, cerebral aneurysms and CNS lymphoma. As AIDS patients live longer, newer and more effective drugs to combat the neurological effects of HIV infection will be required. There is little evidence that HIV damages neurons directly; rather, the damage appears to occur indirectly via viral proteins or neurotoxic factors causing excessive stimulation by excitatory amino acids such as glutamate and quinolinate. This common pathway is similar to that seen in acute neuronal injury and CNS degenerative diseases and may make HIV encephalopathy amenable to pharmacotherapy. The very complexity of HIV CNS entry mechanisms and neuropathogenesis provides a host of sites for potential therapeutic interventions and hope for the future.