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

Changbo Qu; Yang Li; Yunlong Li; Yihang Pan

doi:10.1007/s00705-022-05415-9

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

Changbo Qu, Yang Li, Yunlong Li, Yihang Pan^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › Academic › peer-review

Abstract

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.

Original language	English
Pages (from-to)	1293-1300
Number of pages	8
Journal	Archives of Virology
Volume	167
Issue number	5
DOIs	https://doi.org/10.1007/s00705-022-05415-9
Publication status	Published - May 2022

Bibliographical note

Acknowledgements
This research was supported by the research start-up fund of the Seventh Affiliated Hospital Sun Yat-sen University (SAHSYSU) (ZSQYRSFPD0028) to C. Qu.

Publisher Copyright: © 2022, The Author(s).

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Cite this

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

abstract = "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.",

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

Abstract

Bibliographical note

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