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

Abstract

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.

Cell entry of bovine respiratory syncytial virus through clathrin-mediated endocytosis is regulated by PI3K-Akt and Src-JNK pathways

“…During virus entry via macropinocytosis, the formation of membrane ruffles depends on actin rearrangement, p21-activated kinase 1 (Pak1) is a member of the PAK family and promotes actin rearrangement ( Han et al, 2016 ). To further determine the dependence of BRSV entry into MDBK cells on macropinocytosis, we treated MDBK cells with the Pak1 inhibitor, IPA-3 ( Li et al, 2021 ). The result of cell viability showed that IPA-3 greater than 15 μM inhibited the viability of MDBK cells ( Figure 5E ).…”

Inhibiting retinoic acid signaling in dendritic cells suppresses respiratory syncytial virus infection through enhanced antiviral immunity

“… 41 , 42 Lastly, viral entry and replication pathways were examined, and data indicated downregulation in several genes that have been associated with the entry and replication of many viruses ( Figure 6 E) (TRIM25, cav1, oas2, oasl1, dicer1, and PTX3). 43 , 44 , 45 , 46 , 47 , 48 We also compared the basal gene expression of these pathways in untreated WT and CD11c-dnRARα BMDCs ( Figure S8 ). We found, in comparison to WT, CD11c-dnRARα DCs have higher expression of genes related to innate and adaptive pathways while inflammatory pathway was overall down.…”

IFITM2 Presents Antiviral Response through Enhancing Type I IFN Signaling Pathway

“…A previous study had shown that EMCV infection is associated with the caveolar/lipid raft-dependent endocytic pathway [18]. In addition, both Rab5 and Rab7 are required for endocytosis.…”