Targeting the miR-3156-3p/K+ channel axis suppresses viral release and paralysis in enterovirus D68 infection.

Authors

Yueh-Te Lin, Yu-An Kung, Yu-Nong Gong, Huan-Jung Chiang, Kuei-Ching Hsiung, Hou-Chen Lee, Wen-Fang Tang, Chung-Guei Huang, Jim-Tong Horng, Shin-Ru Shih

Published in

Molecular therapy : the journal of the American Society of Gene Therapy. Sep 30, 2026. Epub Sep 30, 2026.

Abstract

Viruses rely on egress machinery to exit cells, a step that is crucial for their transmission. While non-enveloped RNA viruses, such as enteroviruses, are typically associated with the lytic release pathway, emerging evidence suggests they can also be packaged within vesicles for non-lytic release. However, the molecular mechanisms that regulate viral release remain unclear. Here, we performed a genome-wide CRISPR-Cas9 screen in A549 cells and identified the microRNA hsa-miR-3156-1 as a critical host factor for enterovirus infection. Both the primary and mature forms of miR-3156-1 were upregulated following infection, with miR-3156-3p acting as a positive regulator of viral infection by directly targeting the 3'-untranslated regions of the K⁺ channel-associated genes KCNV1, KCNJ2, KCNK3, and KCNK5, thereby causing plasma membrane depolarization and Ca²⁺ influx, which increase viral release. Pre-administration of a miR-3156-3p antagomir alleviated virus-associated acute flaccid paralysis in an ICR neonatal mouse model. Our findings reveal how the miR-3156-3p/K⁺ channel axis controls enterovirus release, highlighting potential prophylactic targets.

PMID:
42817166
Bibliographic data and abstract were imported from PubMed on 01 Oct 2026.

Read full publication at:
Please sign in to see all details.

Stats

1-terrible, 9-excellent. How would you rate this publication? Sign in in to submit your rating.

Post a comment

You need to be signed in to post comments. You can sign in here.

Comments

There are no comments yet.