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The TLR4-TRIF Pathway Protects against H5N1 Influenza Virus Infection

descriptionPublicationkeyboard_double_arrow_right Article 01 Jan 2012 English Publisher:American Society for MicrobiologyJournal:Journal of Virology, volume 86, pages 19-24 (issn: 0022-538X, eissn: 1098-5514,

Authors: Kyoko Shinya; Kensuke Miyake; Amie J. Eisfeld; Mutsumi Ito; Akiko Makino; Motoko Tanaka; Yoshihiro Kawaoka;

doi: 10.1128/jvi.06168-11

pmid: 22031950

pmc: PMC3255869

The TLR4-TRIF Pathway Protects against H5N1 Influenza Virus Infection

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Abstract

ABSTRACT Prestimulation of the TLR4 pathway with lipopolysaccharide (LPS) protects mice from lethal infection with H5N1 influenza virus. Here, we reveal that the TLR4-TRIF pathway is required for this protective effect by using mice whose TLR4-related molecules were knocked out. Microarray analysis of primary mouse lung culture cells that were LPS pretreated and infected with an H5N1 virus indicated that TLR3 mRNA was upregulated. Primary lung culture cells of TLR3 knockout mice showed no response to LPS pretreatment against H5N1 virus infection, suggesting that TLR3 is also involved in the preventive effect of LPS. Our data suggest that the TLR4-TRIF axis has an important role in stimulating protective innate immunity against H5N1 influenza A virus infection and that TLR3 signaling is involved in this pathway.

Related Organizations

Japan Science and Technology Agency
Japan
Kobe University
Japan
University of Wisconsin–Oshkosh
United States
University of Tokyo
Japan

Keywords

Mice, Knockout, Influenza A Virus, H5N1 Subtype, Cell Line, Mice, Inbred C57BL, Toll-Like Receptor 4, Adaptor Proteins, Vesicular Transport, Mice, Influenza, Human, Animals, Humans, Lung, Signal Transduction

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	citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).	59
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