Woong-Ki Kim

Publications (3)6.2 Total impact

• Source

  Available from: Laurie L Wellman

  Dataset: JNI 475110

  Christina D Steel, Woong-Ki Kim, Larry D Sanford, Laurie L Wellman, Sandra Burnett, Nico Van Rooijen, Richard P Ciavarra
• Article: Distinct macrophage subpopulations regulate viral encephalitis but not viral clearance in the CNS.

  Christina D Steel, Woong-Ki Kim, Larry D Sanford, Laurie L Wellman, Sandra Burnett, Nico Van Rooijen, Richard P Ciavarra
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  ABSTRACT: Intranasal application of vesicular stomatitis virus (VSV) induces acute encephalitis characterized by a pronounced myeloid and T cell infiltrate. The role of distinct phagocytic populations on VSV encephalitis was therefore examined in this study. Ablation of peripheral macrophages did not impair VSV encephalitis or viral clearance from the brain, whereas, depletion of splenic marginal dendritic cells impaired this response and enhanced morbidity/mortality. Selective depletion of brain perivascular macrophages also suppressed this response without altering viral clearance. Thus, two anatomically distinct phagocytic populations regulate VSV encephalitis in a non-redundant fashion although neither population is essential for viral clearance in the CNS.
  Journal of neuroimmunology 09/2010; 226(1-2):81-92. · 2.84 Impact Factor
• Article: SMAD proteins of oligodendroglial cells regulate transcription of JC virus early and late genes coordinately with the Tat protein of human immunodeficiency virus type 1.

  Michelle R Stettner, Jonas A Nance, Clayton A Wright, Yayoi Kinoshita, Woong-Ki Kim, Susan Morgello, Jay Rappaport, Kamel Khalili, Jennifer Gordon, Edward M Johnson
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  ABSTRACT: JC virus (JCV) is the aetiological agent of progressive multifocal leukoencephalopathy (PML), a fatal, demyelinating disease of the brain affecting people with AIDS. Although immunosuppression is involved in infection of the brain by JCV, a direct influence of human immunodeficiency virus type 1 (HIV-1) has also been established. The Tat protein of HIV-1 has been implicated in activation of the cytokine transforming growth factor (TGF)-beta in HIV-1-infected cells and in stimulating JCV gene transcription and DNA replication in oligodendroglia, the primary central nervous system cell type infected by JCV in PML. This study demonstrated that Tat can cooperate with SMAD proteins, the intracellular effectors of TGF-beta, at the JCV DNA control region (CR) to stimulate JCV gene transcription. Tat stimulated JCV early gene transcription in KG-1 oligodendroglial cells when expressed via transfection or added exogenously. Using chromatin immunoprecipitation, it was shown that exogenous Tat enhanced binding of SMAD2, -3 and -4 and their binding partner Fast1 to the JCV CR in living cells. When SMAD2, -3 and -4 were expressed together, Tat, expressed from plasmid pTat, stimulated transcription from both early and late gene promoters, with the early promoter exhibiting stimulation of >100-fold. Tat, SMAD4 and JCV large T-antigen were all visualized in oligodendroglial cells at the border of an active PML lesion in the cerebral frontal lobe. These results revealed a positive reinforcement system in which the SMAD mediators of the TGF-beta system act cooperatively with Tat to stimulate JCV gene transcription.
  Journal of General Virology 05/2009; 90(Pt 8):2005-14. · 3.36 Impact Factor