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Senecavirus A Entry Into Host Cells Is Dependent on the Cholesterol-Mediated Endocytic Pathway.Front Vet Sci.2022 Apr 8;9:840655.doi: 10.3389/fvets.2022.840655. eCollection 2022

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Meiyu Jia,Mingxia Sun,Yan-Dong Tang,Yu-Yuan Zhang,Haiwei Wang,Xuehui Cai,Fandan Meng


Front Vet Sci.2022 Apr 8;9:840655.doi: 10.3389/fvets.2022.840655. eCollection 2022.


Abstract

Senecavirus A (SVA), an important member of the  Picornaviridae  family, causes vesicular disease in pigs. Here, we generated an EGFP-expressing recombinant SVA re-SVA-EGFP, which exhibited similar growth kinetics to its parental virus. The reporter SVA was used to study the role of pig ANTXR1 (pANTXR1) in SVA infection in a porcine alveolar macrophage cell line (PAM-Tang cells). Knockdown of the pANTXR1 significantly reduced SVA infection and replication in PAM-Tang cells, while re-expression of the pANTXR1 promoted the cell susceptibility to SVA infection. The results indicated that pANTXR1 is a crucial receptor mediating SVA infection. Subsequently, the viral endocytosis pathways for SVA entry into pig cells were investigated and the results showed that cholesterol played an essential role in receptor-mediated SVA entry. Together, these results demonstrated that SVA entered into host cells through the pANTXR1-mediated cholesterol pathway. Our findings provide potential targets to develop antiviral drugs for the prevention of SVA infection in the pig population.


Keywords: SVA; cholesterol; pig ANTXR1; reporter virus; viral entry.

Copyright © 2022 Jia, Sun, Tang, Zhang, Wang, Cai and Meng.


上一篇:Transcriptome profiling in swine macrophages infected with African swine fever virus at single-cell resolution.Proc Natl Acad Sci U S A.2022 May 10;119(19):e2201288119.doi: 10.1073/pnas.2201288119. Epub 2022 May 4
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