Abstract

HIV-1 infection is a worldwide pandemic, with an estimate of one to two million children infected by the end of the decade. The neurologic manifestations of primary HIV-1 infection in children are a major cause of morbidity and contribute to the fatal outcome in this condition. In the United States, HIV-1 is the most frequent cause of dementia in young adults. Because antiretroviral therapies and treatment for opportunistic infections have lengthened the survival time but not eradicated the virus from the central nervous system, it is likely that the incidence of neurologic dysfunction, including HIV-1 dementia, will increase. Available evidence suggests that the HIV-1 virus does not productively infect neurons but rather induces programmed cell death (apoptosis) in neurons by production of neurotoxic factors, including cytokines, phospholipid mediators, and eicosanoids, and HIV-1 gene products from HIV-1-infected macrophages in the brain. Understanding the mechanisms involved in neuronal cell injury and death may lead to new therapeutic interventions for the neurologic dysfunction associated with HIV-1 infection of the developing central nervous system.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.