Caveolin-1 is involved in encephalomyocarditis virus replication in BHK-21 cells

Qiongyi Li,Rongxiu Liu,Jialin Bai,Yang Liu,Kexue Zhao,Shujuan Xu,Ying Ling,Amjad Ali

doi:10.1186/s12985-021-01521-3

Qiongyi Li, Rongxiu Liu + Show 6 more

Open Access

https://doi.org/10.1186/s12985-021-01521-3

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Abstract

BackgroundEncephalomyocarditis virus, member of Cardiovirus genus within Picornaviridae family, is an important pathogen that infects different domestic and wild animals. However, the molecular mechanism of its entry remains unclear. In this study, we investigated the mechanism of EMCV infectivity in relation to endocytic pathway using BHK-21 cells.MethodsThe function of numerous cellular key factors implicated in the various endocytic mechanisms were systematically explored using chemical inhibitors. Furthermore, RNA interference (RNAi) as well as the overexpression of dominant protein combined to virus infectivity assays, and confocal microscopy was used to examine EMCV infection in details.ResultsThe results indicated that the EMCV entry into BHK-21 cells depends on caveolin, dynamin, and actin but not clathrin nor macropinocytosis pathways. The effects of overexpression and knockdown of caveolin-1, one components of the caveolae, was examined on EMCV infection. The results showed that EMCV infection was positive correlation with caveolin-1 expression. Confocal microscopy analysis and internalization assay showed that caveolin-1 is required at the early stage of EMCV infection.ConclusionsCaveolin-1, dynamin, and actin-dependent endocytosis pathways are necessary for EMCV infection in vitro.

Highlights

Encephalomyocarditis virus, member of Cardiovirus genus within Picornaviridae family, is an important pathogen that infects different domestic and wild animals
The role of endocytosis in Encephalomyocarditis virus (EMCV) replication in BHK‐21 cells To elucidate whether the endocytic pathway correlated with EMCV replication in BHK-21 cells, endocytosis specific inhibitors were used
Caveolin‐1 is essential for EMCV infection by involving in internalization To ensure the effect of caveolin-1, we examined the colocalization of virus with caveolin-1 by confocal imaging

Summary

Introduction

Encephalomyocarditis virus, member of Cardiovirus genus within Picornaviridae family, is an important pathogen that infects different domestic and wild animals. We investigated the mechanism of EMCV infectivity in relation to endocytic pathway using BHK21 cells. Many viruses can trigger internalization by activating endocytic process such as macropinocytosis, clathrin-mediated endocytosis (CME) and caveolar/lipid raft-dependent, or clathrin- and caveolae-independent endocytic pathways are utilized by different viruses for their entry and replication in permissive cell [10,11,12]. Members of Picornaviridae family use different endocytic mechanisms for infection to occur. CBV3 enters into HeLa cells using clathrinmediated endocytosis pathway [17] and coxsackie virus A9 entry into A549 cells is mediated by dynamin, β2-microglobulin, and Arf6 [12] while FMDV internalization is by clathrin-dependent pathway [18,19,20]. As one member of this family, little is known about the entry mechanism of EMCV

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