Type I interferon imposes a TSG101/ISG15 checkpoint at the Golgi for glycoprotein trafficking during influenza virus infection.
Type I interferon imposes a TSG101/ISG15 checkpoint at the Golgi for glycoprotein trafficking during influenza virus infection.
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DOI:
10.1016/j.chom.2013.10.011
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发表时间:
2013-11-13
影响因子:
30.3
通讯作者:
Ploegh HL
中科院分区:
文献类型:
--
作者:
Sanyal S;Ashour J;Maruyama T;Altenburg AF;Cragnolini JJ;Bilate A;Avalos AM;Kundrat L;García-Sastre A;Ploegh HL
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 remains 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 haemagglutinin (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 surface display of HA and for infectious virion release. These data support the IFN-induced generation of a Tsg101/ISG15-dependent checkpoint in the secretory pathway that compromises influenza virus release.
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影响因子:
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通讯作者:
Lamb RA
DOI:
10.1073/pnas.0710629105
发表时间:
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影响因子:
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