Progression to Neuropsychological Impairment in Human Immunodeficiency Virus Infection Predicted by Elevated Cerebrospinal Fluid Levels of Human Immunodeficiency Virus RNA

Abstract

THE EVENTS that lead to clinically evident neuropsychological (NP) impairment in individuals with human immunodeficiency virus (HIV) infection are likely to evolve over time, such that significant neuronal injury may cumulate over periods ranging from months to years. Human immunodeficiency virus replication itself may be an early "trigger," rather than a late proximate cause of neural injury. In previous cross-sectional studies, levels of HIV RNA in cerebrospinal fluid (CSF) were elevated in HIV-infected subjects with NP impairment at later stages of disease.^1,2 Such cross-sectional studies do not adequately address the likely substantial delay between exposure of central nervous system (CNS) tissues to replicating HIV and the subsequent onset of NP impairment. In addition, if CSF HIV RNA levels were found to be elevated before the development of NP impairment, a causal link between the two would be supported.