title: The regulation of alpha chemokines during HIV-1 infection and leukocyte activation: relevance for HIV-1-associated dementia.
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 alpha-chemokines and their receptor (CXCR3) expression in relevant virus target cells. Macrophages, lymphocytes, and astrocytes secreted alpha-chemokines after HIV-1 infection and/or immune activation. Lymphocyte CXCR3-mediated chemotactic responses were operative. In all, alpha-chemokine-mediated T cell migration continued after HIV-1 infection and the neuroinflammatory events operative during productive viral replication in brain.
authors.affiliation: Center for Neurovirology and Neurodegenerative Disorders, 985215 Nebraska Medical Center, Omaha, NE 68198-5215, USA.
authors.forename: L
authors.initials: L
authors.lastname: Poluektova
authors.forename: T
authors.initials: T
authors.lastname: Moran
authors.forename: M
authors.initials: M
authors.lastname: Zelivyanskaya
authors.forename: S
authors.initials: S
authors.lastname: Swindells
authors.forename: H E
authors.initials: HE
authors.lastname: Gendelman
authors.forename: Y
authors.initials: Y
authors.lastname: Persidsky
mesh_terms: D015526:AIDS Dementia Complex / Q000097:blood / Q000276:immunology* / Q000503:physiopathology; D000328:Adult; D000368:Aged; D001253:Astrocytes / Q000276:immunology / Q000378:metabolism / Q000821:virology; D001921:Brain / Q000276:immunology / Q000378:metabolism / Q000821:virology; D002478:Cells, Cultured / Q000276:immunology / Q000378:metabolism / Q000821:virology; D054357:Chemokine CXCL10; D054371:Chemokine CXCL11; D054370:Chemokine CXCL9; D019743:Chemokines, CXC / Q000097:blood* / Q000276:immunology / Q000378:metabolism / Q000494:pharmacology; D002634:Chemotaxis, Leukocyte / Q000187:drug effects / Q000502:physiology; D002648:Child; D002675:Child, Preschool; D005333:Fetus; D015497:HIV-1 / Q000276:immunology* / Q000472:pathogenicity; D006801:Humans; D007111:Immunity, Cellular / Q000276:immunology*; D036341:Intercellular Signaling Peptides and Proteins; D007371:Interferon-gamma / Q000494:pharmacology; D007962:Leukocytes / Q000276:immunology* / Q000378:metabolism / Q000821:virology; D008213:Lymphocyte Activation / Q000276:immunology*; D008214:Lymphocytes / Q000276:immunology / Q000378:metabolism / Q000821:virology; D008264:Macrophages / Q000276:immunology / Q000378:metabolism / Q000821:virology; D008875:Middle Aged; D012333:RNA, Messenger / Q000276:immunology / Q000378:metabolism; D054367:Receptors, CXCR3; D019707:Receptors, Chemokine / Q000235:genetics / Q000276:immunology / Q000378:metabolism*
chemical_list: C515202:CXCL11 protein, human; C080810:CXCL9 protein, human; C515187:CXCR3 protein, human; D054357:Chemokine CXCL10; D054371:Chemokine CXCL11; D054370:Chemokine CXCL9; D019743:Chemokines, CXC; D036341:Intercellular Signaling Peptides and Proteins; D012333:RNA, Messenger; D054367:Receptors, CXCR3; D019707:Receptors, Chemokine; D007371:Interferon-gamma