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Modeling senecavirus a replication in immortalized porcine alveolar macrophages triggers a robust interferon-mediated immune response that conversely constrains viral replication.
- Source :
-
Virology . Jan2023, Vol. 578, p141-153. 13p. - Publication Year :
- 2023
-
Abstract
- Senecavirus A (SVA) is a newly emerging causative agent of vesicular diseases in swine characterized with wide genetic diversity and rapid evolution. The lack of immunologically active cell culture model impedes the study of SVA-specific innate immunity. Here, an immortalized porcine alveolar macrophages 3D4/21 strongly and productively supported replication of two SVA strains. To elaborate global and dynamic host immune response, we demonstrated that 3D4/21 intrinsically expressed canonical ISGs which were important for pre-empting viral infection. Moreover, 3D4/21 were constitutively abundant in RIG-I-like receptors (RLRs) RIG-I and MDA5 necessary for sensing RNA virus infection, thereby enabling 3D4/21 cells to establish persistent and efficient antiviral status, in particular the most dramatic and sustained expression of type I/II interferons and inflammatory and innate immune genes critical for constraining SVA replication. Our study reveals a pivotal regulatory connection between virus and host that points to the SVA pathogenesis and potential vaccine development. • The 3D4/21 cells strongly and productively supported SVA infection. • SVA triggered IFNs and inflammatory and innate immune genes. • High level of exogenous RIG-I and MDA5 contributed to boosting IFN response in 3D4/21. • Host IFN antiviral response conversely constrained SVA replication. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 00426822
- Volume :
- 578
- Database :
- Academic Search Index
- Journal :
- Virology
- Publication Type :
- Academic Journal
- Accession number :
- 161100847
- Full Text :
- https://doi.org/10.1016/j.virol.2022.12.001