       Document 0254
 DOCN  M9610254
 TI    Regulation of human immunodeficiency virus type 1 and cytokine gene
       expression in myeloid cells by NF-kappa B/Rel transcription factors.
 DT    9601
 AU    Roulston A; Lin R; Beauparlant P; Wainberg MA; Hiscott J; Terry Fox
       Molecular Oncology Group, Lady Davis Institute for; Medical Research,
       Sir Mortimer B. Davis Jewish General Hospital,; Montreal, Quebec,
       Canada.
 SO    Microbiol Rev. 1995 Sep;59(3):481-505. Unique Identifier : AIDSLINE
       MED/96035700
 AB    CD4+ macrophages in tissues such as lung, skin, and lymph nodes,
       promyelocytic cells in bone marrow, and peripheral blood monocytes serve
       as important targets and reservoirs for human immunodeficiency virus
       type 1 (HIV-1) replication. HIV-1-infected myeloid cells are often
       diminished in their ability to participate in chemotaxis, phagocytosis,
       and intracellular killing. HIV-1 infection of myeloid cells can lead to
       the expression of surface receptors associated with cellular activation
       and/or differentiation that increase the responsiveness of these cells
       to cytokines secreted by neighboring cells as well as to bacteria or
       other pathogens. Enhancement of HIV-1 replication is related in part to
       increased DNA-binding activity of cellular transcription factors such as
       NF-kappa B. NF-kappa B binds to the HIV-1 enhancer region of the long
       terminal repeat and contributes to the inducibility of HIV-1 gene
       expression in response to multiple activating agents. Phosphorylation
       and degradation of the cytoplasmic inhibitor I kappa B alpha are crucial
       regulatory events in the activation of NF-kappa B DNA-binding activity.
       Both N- and C-terminal residues of I kappa B alpha are required for
       inducer-mediated degradation. Chronic HIV-1 infection of myeloid cells
       leads to constitutive NF-kappa B DNA-binding activity and provides an
       intranuclear environment capable of perpetuating HIV-1 replication.
       Increased intracellular stores of latent NF-kappa B may also result in
       rapid inducibility of NF-kappa B-dependent cytokine gene expression. In
       response to secondary pathogenic infections or antigenic challenge,
       cytokine gene expression is rapidly induced, enhanced, and sustained
       over prolonged periods in HIV-1-infected myeloid cells compared with
       uninfected cells. Elevated levels of several inflammatory cytokines have
       been detected in the sera of HIV-1-infected individuals. Secretion of
       myeloid cell-derived cytokines may both increase virus production and
       contribute to AIDS-associated disorders.
 DE    Base Sequence  Cytokines/BIOSYNTHESIS/GENETICS/*PHYSIOLOGY  CD4-Positive
       T-Lymphocytes/VIROLOGY  Disease Progression  Gene Products,
       tat/PHYSIOLOGY  Human  HIV
       Infections/COMPLICATIONS/PHYSIOPATHOLOGY/THERAPY/*VIROLOGY
       HIV-1/*PHYSIOLOGY/PATHOGENICITY  Leukocytes/*PHYSIOLOGY/VIROLOGY
       Macrophages/*PHYSIOLOGY/VIROLOGY  Molecular Sequence Data  NF-kappa
       B/*PHYSIOLOGY  Phosphorylation  Support, Non-U.S. Gov't  Transcription,
       Genetic/*PHYSIOLOGY  Virus Replication/PHYSIOLOGY  JOURNAL ARTICLE
       REVIEW  REVIEW, TUTORIAL

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

