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


Journal

Virology journal
ISSN: 1743-422X
Titre abrégé: Virol J
Pays: England
ID NLM: 101231645

Informations de publication

Date de publication:
24 03 2021
Historique:
received: 23 10 2020
accepted: 02 03 2021
entrez: 25 3 2021
pubmed: 26 3 2021
medline: 23 2 2022
Statut: epublish

Résumé

Encephalomyocarditis 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. The 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. The 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. Caveolin-1, dynamin, and actin-dependent endocytosis pathways are necessary for EMCV infection in vitro.

Sections du résumé

BACKGROUND
Encephalomyocarditis 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.
METHODS
The 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.
RESULTS
The 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.
CONCLUSIONS
Caveolin-1, dynamin, and actin-dependent endocytosis pathways are necessary for EMCV infection in vitro.

Identifiants

pubmed: 33761945
doi: 10.1186/s12985-021-01521-3
pii: 10.1186/s12985-021-01521-3
pmc: PMC7989721
doi:

Substances chimiques

Actins 0
Caveolin 1 0
Dynamins EC 3.6.5.5

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

63

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Auteurs

Qiongyi Li (Q)

Biomedical Research Center, Key Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Northwest Minzu University, Lanzhou, China.
College of Life Science and Engineering, Northwest Minzu University, Lanzhou, China.

Yang Liu (Y)

Biomedical Research Center, Key Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Northwest Minzu University, Lanzhou, China.
College of Life Science and Engineering, Northwest Minzu University, Lanzhou, China.

Shujuan Xu (S)

Biomedical Research Center, Key Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Northwest Minzu University, Lanzhou, China.
College of Life Science and Engineering, Northwest Minzu University, Lanzhou, China.

Kexue Zhao (K)

Biomedical Research Center, Key Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Northwest Minzu University, Lanzhou, China.
College of Life Science and Engineering, Northwest Minzu University, Lanzhou, China.

Ying Ling (Y)

College of Life Science and Engineering, Northwest Minzu University, Lanzhou, China.

Rongxiu Liu (R)

College of Life Science and Engineering, Northwest Minzu University, Lanzhou, China.

Amjad Ali (A)

Biomedical Research Center, Key Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Northwest Minzu University, Lanzhou, China.

Jialin Bai (J)

Biomedical Research Center, Key Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Northwest Minzu University, Lanzhou, China. jlbai@xbmu.edu.cn.
College of Life Science and Engineering, Northwest Minzu University, Lanzhou, China. jlbai@xbmu.edu.cn.

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