Mice Lacking the ISG15 E1 Enzyme UbE1L Demonstrate Increased Susceptibility to both Mouse-Adapted and Non-Mouse-Adapted Influenza B Virus Infection

被引：110

作者：

Lai, Caroline ^{[1
]}

Struckhoff, Jessica J. ^{[1
]}

Schneider, Jana ^{[3
]}

Martinez-Sobrido, Luis ^{[4
,5
]}

Wolff, Thorsten ^{[3
]}

Garcia-Sastre, Adolfo ^{[4
,5
,6
]}

Zhang, Dong-Er ^{[7
]}

Lenschow, Deborah J. ^{[1
,2
]}

机构：

[1] Washington Univ, Sch Med, Dept Internal Med, St Louis, MO 63110 USA

[2] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA

[3] Robert Koch Inst, D-13353 Berlin, Germany

[4] Mt Sinai Sch Med, Dept Microbiol, New York, NY 10029 USA

[5] Mt Sinai Sch Med, Div Infect Dis, Dept Med, New York, NY 10029 USA

[6] Mt Sinai Sch Med, Emerging Pathogens Inst, New York, NY 10029 USA

[7] Scripps Res Inst, La Jolla, CA 92037 USA

来源：

JOURNAL OF VIROLOGY | 2009年 / 83卷 / 02期

关键词：

INTERFERON-STIMULATED GENE-15; NS1; PROTEIN; ANTIVIRAL MOLECULE; UBIQUITIN E2; IDENTIFICATION; CONJUGATION; LIGASE; ISGYLATION; INDUCTION; SECRETION;

D O I：

10.1128/JVI.00105-08

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

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.

引用

页码：1147 / 1151

页数：5

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