Herpes simplex virus-1 infection causes the secretion of a type I interferon-antagonizing protein and inhibits signaling at or before Jak-1 activation

Journal Article · Tue Jan 05 04:00:00 EST 2010 · Virology

DOI:https://doi.org/10.1016/j.virol.2009.09.021· OSTI ID:21357579

Johnson, Karen E ^[1]

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1. Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115 (United States)

Host cells respond to viral infection by the production of type I interferons (IFNs), which induce the expression of antiviral genes. Herpes simplex virus I (HSV-1) encodes many mechanisms that inhibit the type I IFN response, including the ICP27-dependent inhibition of type I IFN signaling. Here we show inhibition of Stat-1 nuclear accumulation in cells that express ICP27. ICP27 expression also induces the secretion of a small, heat-stable type I IFN antagonizing protein that inhibits Stat-1 nuclear accumulation. We show that the inhibition of IFN-induced Stat-1 phosphorylation occurs at or upstream of Jak-1 phosphorylation. Finally, we show that ISG15 expression is induced after IFNalpha treatment in mock-infected cells, but not cells infected with WT HSV-1 or ICP27{sup -} HSV-1. These data suggest that HSV-1 has evolved multiple mechanisms to inhibit IFN signaling not only in infected cells, but also in neighboring cells, thereby allowing for increased viral replication and spread.

• OSTI ID: 21357579
• Journal Information: Virology, Journal Name: Virology Journal Issue: 1 Vol. 396; ISSN VIRLAX; ISSN 0042-6822
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
BUILDUP
CHEMICAL REACTIONS
DISEASES
GENES
GROWTH FACTORS
HERPES SIMPLEX
INFECTIOUS DISEASES
INHIBITION
INTERFERON
LYMPHOKINES
MICROORGANISMS
MITOGENS
ORGANIC COMPOUNDS
PARASITES
PHOSPHORYLATION
PROTEINS
SECRETION
SKIN DISEASES
VIRAL DISEASES
VIRUSES