Mice lacking the ISG15 E1 enzyme UbE1L demonstrate increased susceptibility to both mouse-adapted and non-mouse-adapted influenza B virus infection

Caroline Lai, Jessica J. Struckhoff, Jana Schneider, Luis Martinez-Sobrido, Thorsten Wolff, Adolfo García-Sastre, Dong Er Zhang, Deborah J. Lenschow

Research output: Contribution to journalArticle

89 Scopus citations

Abstract

ISG15 functions as a critical antiviral molecule against influenza virus, with infection inducing both the conjugation of ISG15 to target proteins and production of free ISG15. Here, we report that mice lacking the ISG15 E1 enzyme UbE1L fail to form ISG15 conjugates. Both UbE1L-/- and ISG15 -/- mice display increased susceptibility to influenza B virus infection, including non-mouse-adapted strains. Finally, we demonstrate that ISG15 controls influenza B virus infection through its action within radioresistant stromal cells and not bone marrow-derived cells. Thus, the conjugation of ISG15 to target proteins within stromal cells is critical to its activity against influenza virus.

Original languageEnglish
Pages (from-to)1147-1151
Number of pages5
JournalJournal of virology
Volume83
Issue number2
DOIs
StatePublished - Jan 1 2009

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