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[转移帖]Nat Immunol.:揭示干扰素抗病毒新机制——“外体”

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发布时间: 2015-6-4 17:11

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本帖最后由 ipsvirus 于 2015-6-4 17:12 编辑    原帖由ipsvirus于2013-7-8 14:14 发于老论坛     上海医学院基础医学院教育部、卫生部医学分子病毒学重点实验室主任袁正宏研究员率领课题组 ...

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ipsvirus 发表于 2015-6-4 18:14:55
exosomes在这几年还是挺火的。感染的免疫细胞可以通过分泌胞内体,将一些抗病毒成分,比如蛋白分子,核酸分子等带到组织细胞中,来发挥抗病毒作用。

还有很多文章报道了类似机制。

Proc Natl Acad Sci U S A. 2014 Nov 18;111(46):E4991-6. doi: 10.1073/pnas.1419338111. Epub 2014 Nov 3.

Cells infected with herpes simplex virus 1 export to uninfected cells exosomes containing STING, viral mRNAs, and microRNAs.
Kalamvoki M1, Du T1, Roizman B2.

Abstract
STING (stimulator of IFN genes) activates the IFN-dependent innate immune response to infection on sensing the presence of DNA in cytosol. The quantity of STING accumulating in cultured cells varies; it is relatively high in some cell lines [e.g., HEp-2, human embryonic lung fibroblasts (HEL), and HeLa] and low in others (e.g., Vero cells). In a preceding publication we reported that STING was stable in four cell lines infected with herpes simplex virus 1 and that it was actively stabilized in at least two cell lines derived from human cancers. In this report we show that STING is exported from HEp-2 cells to Vero cells along with virions, viral mRNAs, microRNAs, and the exosome marker protein CD9. The virions and exosomes copurified. The quantity of STING and CD9 exported from one cell line to another was inoculum-size-dependent and reflected the levels of STING and CD9 accumulating in the cells in which the virus inoculum was made. The export of STING, an innate immune sensor, and of viral mRNAs whose major role may be in silencing viral genes in latently infected neurons, suggests that the virus has evolved mechanisms that curtail rather than foster the spread of infection under certain conditions.
ipsvirus 发表于 2015-6-4 17:54:53
Exosomes mediate the cell-to-cell transmission of IFN-α-induced antiviral activity

Jianhua Li, Kuancheng Liu, Yang Liu, Yan Xu, Fei Zhang, Huijuan Yang, Jiangxia Liu, Tingting Pan, Jieliang Chen, Min Wu, Xiaohui Zhou        & Zhenghong Yuan

The cell-to-cell transmission of viral resistance is a potential mechanism for amplifying the interferon-induced antiviral response. In this study, we report that interferon-α (IFN-α) induced the transfer of resistance to hepatitis B virus (HBV) from nonpermissive liver nonparenchymal cells (LNPCs) to permissive hepatocytes via exosomes. Exosomes from IFN-α-treated LNPCs were rich in molecules with antiviral activity. Moreover, exosomes from LNPCs were internalized by hepatocytes, which mediated the intercellular transfer of antiviral molecules. Finally, we found that exosomes also contributed to the antiviral response of IFN-α to mouse hepatitis virus A59 and adenovirus in mice. Thus, we propose an antiviral mechanism of IFN-α activity that involves the induction and intercellular transfer of antiviral molecules via exosomes.

http://www.nature.com/ni/journal ... mentary-information

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