The regulation of alpha chemokines during HIV-1 infection and leukocyte activation: Relevance for HIV-1-associated dementia

Larisa Y Poluektova, Tim Moran, Marina Zelivyanskaya, Susan Swindells, Howard Eliot Gendelman, Yuri Persidsky

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

Cellular immunity against human immunodeficiency virus type 1 (HIV-1)-infected brain macrophages serves to prevent productive viral replication in the nervous system. Inevitably, during advanced disease, this antiretroviral response breaks down. This could occur through virus-induced dysregulation of lymphocyte trafficking. Thus, we studied the production of non-ELR-containing α-chemokines and their receptor (CXCR3) expression in relevant virus target cells. Macrophages, lymphocytes, and astrocytes secreted α-chemokines after HIV-1 infection and/or immune activation. Lymphocyte CXCR3-mediated chemotactic responses were operative. In all, α-chemokine-mediated T cell migration continued after HIV-1 infection and the neuroinflammatory events operative during productive viral replication in brain.

Original languageEnglish (US)
Pages (from-to)112-128
Number of pages17
JournalJournal of Neuroimmunology
Volume120
Issue number1-2
DOIs
StatePublished - Nov 10 2001

Fingerprint

CXC Chemokines
Virus Diseases
Dementia
HIV-1
Leukocytes
Lymphocytes
Chemokines
Macrophages
Viruses
Chemokine Receptors
Brain
Cellular Immunity
Astrocytes
Nervous System
Cell Movement
T-Lymphocytes

Keywords

  • Brain
  • Chemotaxis
  • HIV-1 infection
  • Lymphocyte
  • Monocyte/macrophage

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

Cite this

The regulation of alpha chemokines during HIV-1 infection and leukocyte activation : Relevance for HIV-1-associated dementia. / Poluektova, Larisa Y; Moran, Tim; Zelivyanskaya, Marina; Swindells, Susan; Gendelman, Howard Eliot; Persidsky, Yuri.

In: Journal of Neuroimmunology, Vol. 120, No. 1-2, 10.11.2001, p. 112-128.

Research output: Contribution to journalArticle

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