HIV-associated neurocognitive disease continues in the antiretroviral era.
Despite the ability to suppress viral replication with antiretroviral therapy, HIV-associated neurocognitive disturbances can still be detected in nearly half of patients. Neurologic dysfunction before initiating or in the absence of antiretroviral treatment is primarily the result of neuronal dysfunction or loss from direct viral effects, whereas that in patients receiving antiretroviral therapy appears to be associated at least in part with inflammation driven by chronic low-level infection. Contributing factors may include genetic differences in HIV and human hosts and aging of patients. This article summarizes a presentation on HIV-associated neurocognitive disorder made by David B. Clifford, MD, at an International AIDS Society-USA Continuing Medical Education course in New York in October 2007.
Clifford
David B
DB
Washington University School of Medicine, Saint Louis, MO, USA.
D019380:Anti-HIV Agents / Q000009:adverse effects* / Q000494:pharmacology / Q000627:therapeutic use; D023241:Antiretroviral Therapy, Highly Active; D003072:Cognition Disorders / Q000209:etiology* / Q000821:virology*; D015658:HIV Infections / Q000150:complications* / Q000188:drug therapy / Q000821:virology; D015497:HIV-1 / Q000187:drug effects* / Q000235:genetics; D006801:Humans
D019380:Anti-HIV Agents