Cargando…
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...
Autores principales: | , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Vienna
2022
|
Materias: | |
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 |
_version_ | 1784673387245731840 |
---|---|
author | Qu, Changbo Li, Yang Li, Yunlong Pan, Yihang |
author_facet | Qu, Changbo Li, Yang Li, Yunlong Pan, Yihang |
author_sort | Qu, Changbo |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-8942808 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Springer Vienna |
record_format | MEDLINE/PubMed |
spelling | pubmed-89428082022-03-24 Full-length MAVS, a mitochondrial antiviral-signaling protein, inhibits hepatitis E virus replication, requiring JAK-STAT signaling Qu, Changbo Li, Yang Li, Yunlong Pan, Yihang Arch Virol Brief Report 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. Springer Vienna 2022-03-24 2022 /pmc/articles/PMC8942808/ /pubmed/35322318 http://dx.doi.org/10.1007/s00705-022-05415-9 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Brief Report Qu, Changbo Li, Yang Li, Yunlong Pan, Yihang Full-length MAVS, a mitochondrial antiviral-signaling protein, inhibits hepatitis E virus replication, requiring JAK-STAT signaling |
title | Full-length MAVS, a mitochondrial antiviral-signaling protein, inhibits hepatitis E virus replication, requiring JAK-STAT signaling |
title_full | Full-length MAVS, a mitochondrial antiviral-signaling protein, inhibits hepatitis E virus replication, requiring JAK-STAT signaling |
title_fullStr | Full-length MAVS, a mitochondrial antiviral-signaling protein, inhibits hepatitis E virus replication, requiring JAK-STAT signaling |
title_full_unstemmed | Full-length MAVS, a mitochondrial antiviral-signaling protein, inhibits hepatitis E virus replication, requiring JAK-STAT signaling |
title_short | Full-length MAVS, a mitochondrial antiviral-signaling protein, inhibits hepatitis E virus replication, requiring JAK-STAT signaling |
title_sort | full-length mavs, a mitochondrial antiviral-signaling protein, inhibits hepatitis e virus replication, requiring jak-stat signaling |
topic | Brief Report |
url | 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 |
work_keys_str_mv | AT quchangbo fulllengthmavsamitochondrialantiviralsignalingproteininhibitshepatitisevirusreplicationrequiringjakstatsignaling AT liyang fulllengthmavsamitochondrialantiviralsignalingproteininhibitshepatitisevirusreplicationrequiringjakstatsignaling AT liyunlong fulllengthmavsamitochondrialantiviralsignalingproteininhibitshepatitisevirusreplicationrequiringjakstatsignaling AT panyihang fulllengthmavsamitochondrialantiviralsignalingproteininhibitshepatitisevirusreplicationrequiringjakstatsignaling |