HIV-1 encephalopathy among perinatally infected children: Neuropathogenesis and response to highly active antiretroviral therapy

Research output: Contribution to journalReview article

19 Scopus citations

Abstract

HIV-1 encephalopathy among perinatally infected children in the United States was initially defined by a classic triad of findings that included: (1) developmental delay, (2) secondary or acquired microcephaly, and (3) pyramidal tract neuromotor deficits. The most severe form of this disorder typically occurred among young children who developed rapidly progressive disease in concert with profound immunosuppression, and Pneumocystis jiroveci pneumonitis (PCP). The neuropathogenesis of this disorder appears to involve a cascade of viral products, various cytokines and chemokines, and neurotransmitters which promote ongoing inflammation, excitation, and overstimulation of the N-methyl-D-aspartate type receptor (NMDAR) system. These subsequently lead to neuronal injury and death secondary to apoptosis or necrosis, astrocytosis, as well as dentritic and synaptic damage. The frequency of the most severe forms of encephalopathy among children has dropped dramatically since the introduction of highly active antiretroviral therapy (HAART). Of concern, however, is the possibility that a more insidious form of this disorder may be occurring presently among older vertically infected children as a result of inadequate penetration of HAART agents into the cerebrospinal fluid (CSF). This paper will review what published data there is as yet that bears on this question.

Original languageEnglish (US)
Pages (from-to)216-222
Number of pages7
JournalMental Retardation and Developmental Disabilities Research Reviews
Volume12
Issue number3
DOIs
StatePublished - Nov 3 2006

Keywords

  • Central nervous system (CNS) neuropathogenesis
  • HAART
  • HIV encephalopathy

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Neuropsychology and Physiological Psychology
  • Genetics(clinical)

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