Document 0584
 DOCN  M9460584
 TI    Regulation of interferon-alpha-inducible cellular genes in human
       immunodeficiency virus-infected monocytes.
 DT    9404
 AU    Baca LM; Genis P; Kalvakolanu D; Sen G; Meltzer MS; Zhou A; Silverman R;
       Gendelman HE; Department of Medicine, University of Nebraska Medical
       Center,; Omaha 68194.
 SO    J Leukoc Biol. 1994 Mar;55(3):299-309. Unique Identifier : AIDSLINE
       MED/94165565
 AB    Cellular mechanisms that control susceptibility to opportunistic
       infection in human immunodeficiency virus (HIV)-infected individuals
       remain poorly understood. HIV may induce certain cellular genes that
       restrict HIV replication and protect cells against other superinfecting
       viral pathogens. Indeed, HIV-infected monocytes resist infection by
       vesicular stomatitis virus (VSV). HIV-induced VSV interference in
       monocytes increases with time after HIV infection. Such interference was
       evident 6 h after HIV infection and reached maximal levels at 14 days.
       Monocytotropic but not T cell-tropic HIV strains elicited these effects,
       signaling a requirement for viral entry and/or replication. Viral
       interference was independent of interferon (IFN) and was unaffected by
       addition of neutralizing IFN-alpha and -beta antibodies. The
       well-described IFN-alpha-inducible antiviral pathways were examined to
       determine their relationship to the cellular mechanism(s) underlying VSV
       interference. HIV and IFN-alpha both induced the expression of 2-5A
       synthetase and Mx gene. In contrast, the guanylate-binding protein
       (GBP), 6-16, and 9-27 cellular genes were up-regulated by IFN-alpha but
       not HIV. MxA was detected in HIV-infected monocytes but not in
       uninfected monocytes. The association between Mx expression and
       resistance to VSV, coupled with previously described anti-VSV activities
       by human MxA, suggested that Mx may be an effector molecule for the
       HIV-induced anti-VSV activities. These results, taken together, suggest
       that HIV can induce antiviral cellular gene expression, independent of
       IFN.
 DE    Base Sequence  Blotting, Northern  Cells, Cultured
       Cycloheximide/PHARMACOLOGY  DNA/ANALYSIS/GENETICS  Fluorescent Antibody
       Technique  Gene Expression Regulation/*DRUG EFFECTS/PHYSIOLOGY  Human
       HIV/*ISOLATION & PURIF/PHYSIOLOGY  HIV Infections/*PHYSIOPATHOLOGY
       Interferon-alpha/*PHARMACOLOGY  Interferons/METABOLISM/PHYSIOLOGY
       Molecular Sequence Data  Monocytes/*CYTOLOGY/ENZYMOLOGY/*MICROBIOLOGY
       Polymerase Chain Reaction/METHODS  Proteins/ANALYSIS/GENETICS/PHYSIOLOGY
       Reverse Transcriptase  Support, Non-U.S. Gov't  Support, U.S. Gov't,
       P.H.S.  Up-Regulation (Physiology)  Vesicular Stomatitis-Indiana
       Virus/PHYSIOLOGY  Virus Inhibitors/ANALYSIS/GENETICS/PHYSIOLOGY
       2',5'-Oligoadenylate Synthetase/ANALYSIS  JOURNAL ARTICLE

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