Full-length MAVS, a mitochondrial antiviral-signaling protein, inhibits hepatitis E virus replication, requiring JAK-STAT signaling

Hepatitis E virus (HEV) infection is the leading cause of acute hepatitis worldwide. The mitochondrial antiviral signaling protein (MAVS)-mediated interferon (IFN) response plays a pivotal role in hepatic antiviral immunity. However, little is known about the effect of overexpression of MAVS on HEV...

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Detalles Bibliográficos
Autores principales: Qu, Changbo, Li, Yang, Li, Yunlong, Pan, Yihang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Vienna 2022
Materias:
Brief Report
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8942808/
https://www.ncbi.nlm.nih.gov/pubmed/35322318
http://dx.doi.org/10.1007/s00705-022-05415-9
Descripción
Sumario:Hepatitis E virus (HEV) infection is the leading cause of acute hepatitis worldwide. The mitochondrial antiviral signaling protein (MAVS)-mediated interferon (IFN) response plays a pivotal role in hepatic antiviral immunity. However, little is known about the effect of overexpression of MAVS on HEV infection. Full-length MAVS (FL-MAVS) is the main form of MAVS that increases the production of IFNs. Here, we studied the effect of FL-MAVS on HEV infection. We found that overexpression of FL-MAVS profoundly inhibited HEV replication. Furthermore, we showed that the anti-HEV effect of FL-MAVS is largely dependent on JAK-STAT signaling activation. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s00705-022-05415-9.

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