Giuseppe
Emeritus
J Virol. 2008 Nov 12. [Epub ahead of print]
Mice lacking the ISG15 E1 enzyme, UbE1L, demonstrate increased susceptibility to both mouse adapted and non-adapted influenza B virus infection.
Lai C, Struckhoff JJ, Schneider J, Martinez-Sobrido L, Wolff T, Garc?a-Sastre A, Zhang DE, Lenschow DJ. - Department of Internal Medicine, Pathology & Immunology, Washington University School of Medicine, St. Louis, MO 63110; Robert Koch-Institute, P15, 13353 Berlin, Germany; Department of Microbiology, Department of Medicine, Division of Infectious Diseases, and Emerging Pathogens Institute, Mount Sinai School of Medicine, New York City, NY 10029; The Scripps Research Institute, LaJolla, CA.
ISG15 functions as a critical antiviral molecule against influenza virus, with infection inducing both the ISGylation of 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 antiviral activity against influenza virus.
PMID: 19004958 [PubMed - as supplied by publisher]
-
------
Mice lacking the ISG15 E1 enzyme, UbE1L, demonstrate increased susceptibility to both mouse adapted and non-adapted influenza B virus infection.
Lai C, Struckhoff JJ, Schneider J, Martinez-Sobrido L, Wolff T, Garc?a-Sastre A, Zhang DE, Lenschow DJ. - Department of Internal Medicine, Pathology & Immunology, Washington University School of Medicine, St. Louis, MO 63110; Robert Koch-Institute, P15, 13353 Berlin, Germany; Department of Microbiology, Department of Medicine, Division of Infectious Diseases, and Emerging Pathogens Institute, Mount Sinai School of Medicine, New York City, NY 10029; The Scripps Research Institute, LaJolla, CA.
ISG15 functions as a critical antiviral molecule against influenza virus, with infection inducing both the ISGylation of 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 antiviral activity against influenza virus.
PMID: 19004958 [PubMed - as supplied by publisher]
-
------