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Exosomes exploit the virus entry machinery and pathway to transmit IFN-α-induced antiviral activity.

By Zhenlan Yao, Xiaofang Li, Jieliang Chen, Yunsheng Qiao, Fang Shen, Bisheng Shi, Jia Liu, Jiahui Ding, Lu Peng, Jianhua Li, Zhenghong Yuan

Posted 13 Apr 2018
bioRxiv DOI: 10.1101/300715 (published DOI: 10.1128/JVI.01578-18)

Interferon-α (IFN-α) induces the transfer of resistance to hepatitis B virus (HBV) from liver nonparenchymal cells (LNPCs) to hepatocytes via exosomes. However, little is known about the entry machinery and pathway involved in the transmission of IFN-α-induced antiviral activity. Here, we found that macrophage exosomes depend on T cell immunoglobulin and mucin receptor 1 (TIM-1), a hepatitis A virus (HAV) receptor, to enter hepatocytes for delivering IFN-α-induced anti-HBV activity. Moreover, two primary endocytic routes for virus infection, clathrin-mediated endocytosis (CME) and macropinocytosis, collaborate to permit exosome entry and anti-HBV activity transfer. Subsequently, lysobisphosphatidic acid (LBPA), an anionic lipid closely related to endosome penetration of virus, facilitates membrane fusion of exosomes in late endosomes/multivesicular bodies (LEs/MVBs) and the accompanying exosomal cargo uncoating. Together, this study provides comprehensive insights into the transmission route of macrophage exosomes to efficiently deliver IFN-α-induced anti-HBV activity and highlights the similarities between the entry mechanisms of exosomes and virus.

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