Type i interferon imposes a TSG101/ISG15 checkpoint at the Golgi for glycoprotein trafficking during influenza virus infection

Sumana Sanyal, Joseph Ashour, Takeshi Maruyama, Arwen F. Altenburg, Juan Jose Cragnolini, Angelina Bilate, Ana M. Avalos, Lenka Kundrat, Adolfo García-Sastre, Hidde L. Ploegh*

*この研究の対応する著者

研究成果: Article査読

26 被引用数 (Scopus)

抄録

Several enveloped viruses exploit host pathways, such as the cellular endosomal sorting complex required for transport (ESCRT) machinery, for their assembly and release. The influenza A virus (IAV) matrix protein binds to the ESCRT-I complex, although the involvement of early ESCRT proteins such as Tsg101 in IAV trafficking remain to be established. We find that Tsg101 can facilitate IAV trafficking, but this is effectively restricted by the interferon (IFN)-stimulated protein ISG15. Cytosol from type I IFN-treated cells abolished IAV hemagglutinin (HA) transport to the cell surface in infected semi-intact cells. This inhibition required Tsg101 and could be relieved with deISGylases. Tsg101 is itself ISGylated in IFN-treated cells. Upon infection, intact Tsg101-deficient cells obtained by CRISPR-Cas9 genome editing were defective in the surface display of HA and for infectious virion release. These data support the IFN-induced generation of a Tsg101- and ISG15-dependent checkpoint in the secretory pathway that compromises influenza virus release.

本文言語English
ページ(範囲)510-521
ページ数12
ジャーナルCell Host and Microbe
14
5
DOI
出版ステータスPublished - 2013 11 13
外部発表はい

ASJC Scopus subject areas

  • 寄生虫科
  • 微生物学
  • ウイルス学

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