Exosomes from EV71-infected oral epithelial cells can transfer miR-30a to promote EV71 infection.

Exosomes from EV71-infected oral epithelial cells can transfer miR-30a to promote EV71 infection.:

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Exosomes from EV71-infected oral epithelial cells can transfer miR-30a to promote EV71 infection.

Oral Dis. 2020 Jan 20;:

Authors: Wang Y, Zhang S, Song W, Zhang W, Li J, Li C, Qiu Y, Fang Y, Jiang Q, Li X, Yan B

Abstract

OBJECTIVE: As an extracellular vesicles, exosomes can release from virus infected cells contain various viral or host cellular elements and could stimulate recipient's cellular response. Enterovirus 71 (EV71), a single-strand positive sense RNA virus, is known to cause hand, foot, and mouth disease (HFMD) in children and bring about severe clinical diseases.

METHODS: Separated the human oral epithelial cells (OE cells) from normal buccal mucosa through enzyme digestion. Performed a comprehensive miRNA profiling in exosomes from EV71-infected OE cells through deep small RNA-seq. Using the Human Antiviral Response RT Profiler PCR Array profiles to explore the interactions of innate immune signaling networks with exosomal miR-30a. Knocked out the MyD88 gene in macrophages using CRISPR/Cas9-mediated genome editing method.

RESULTS: Our study demonstrated that the miR-30a was preferentially enriched in exosomes that released from EV71-infected human oral epithelial cells through small RNA-Seq. We found that the transfer of exosomal miR-30a to macrophages could suppress type Ⅰ interferon response through targeting myeloid differentiation factor 88 (MyD88), subsequently facilitate the viral replication.

CONCLUSIONS: Exosomes released from EV71-infected OE cells selectively packaged high level of miR-30a that can be functionally transferred to the recipient macrophages resulted in targeting MyD88, subsequently inhibited type I interferon production in receipt cells, thus promoting the EV71 replication.

PMID: 31958204 [PubMed - as supplied by publisher]