Int J Biol Sci 2019; 15(13):2925-2935. doi:10.7150/ijbs.36388 This issue

Research Paper

Exosomal MicroRNA-155 Inhibits Enterovirus A71 Infection by Targeting PICALM

Jing Wu1,2, Jiaqi Gu1,2, Li Shen3, Daihua Fang4, Xinran Zou1,2, Yuwen Cao1,2, Shengjun Wang1,2, Lingxiang Mao1✉

1. Department of Laboratory Medicine, The Affiliated People's Hospital, Jiangsu University, Zhenjiang, China
2. Department of Immunology, Jiangsu Key Laboratory of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, China
3. Clinical Laboratory, Zhenjiang Center for Disease Control and Prevention, Jiangsu, China
4. Clinical Laboratory, Xuzhou Children's Hospital, Xuzhou, China

This is an open access article distributed under the terms of the Creative Commons Attribution License ( See for full terms and conditions.
Wu J, Gu J, Shen L, Fang D, Zou X, Cao Y, Wang S, Mao L. Exosomal MicroRNA-155 Inhibits Enterovirus A71 Infection by Targeting PICALM. Int J Biol Sci 2019; 15(13):2925-2935. doi:10.7150/ijbs.36388. Available from

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Graphic abstract

Enterovirus A71 (EV-A71) causes hand, foot, and mouth disease (HFMD) that is associated with neurological complications. Researchers have shown that exosomes containing host cellular microRNA (miRNA) can modulate the recipient's cellular response during viral infection. However, it is unclear how exosomal miRNAs regulate this response during EV-A71 infection. In this study, we used an exosomal miRNA chip to show that microRNA-155 (miR-155) was markedly enriched in exosomes after EV-A71 infection. Moreover, exosomal miR-155 efficaciously inhibited EV-A71 infection by targeting phosphatidylinositol clathrin assembly protein (PICALM) in recipient cells. Importantly, we confirmed that exosomal miR-155 reduced EV-A71 infection severity in vivo. Additionally, miR-155 levels in throat swabs from EV-A71-infected patients were higher than in those from healthy individuals. Collectively, our findings provide evidence that exosomal miR-155 plays a role in host-pathogen interactions by mediating EV-A71 infection via the repression of PICALM; these results provide insights into the regulatory mechanisms of viral infection.

Keywords: Enterovirus A71, Exosomes, MicroRNA-155, PICALM