Actomyosin dependent cell contractility orchestrates zika virus infection.

Abstract

Emerging pathogen infections such as Zika virus (ZIKV) pose an increasing threat to human health, but the role of mechanobiological attribute of host cells during ZIKV infection is largely unknown. Here, we revealed that ZIKV infection led to increased contractility of host cells. Importantly, we investigated whether host cell contractility contributes to ZIKV infection efficacy, from both intracellular and extracellular perspective. By performing drug perturbation and gene editing experiments, we confirmed that disruption of contractile actomyosin compromises ZIKV infection efficiency, viral genome replication and viral particle production. By culturing on compliant matrix, we further demonstrated that softer substrate leading to less contractility of host cells compromises ZIKV infection, resemble of disrupting the intracellular actomyosin organization. Together, our work provides evidence to support a positive correlation between host cell contractility and ZIKV infection efficacy, thus unveiling an unprecedented layer of interplay between ZIKV and host cell.