scholarly journals Apolipoprotein E polymorphisms and their protective effect on hepatitis E virus replication

Hepatology ◽  
2016 ◽  
Vol 64 (6) ◽  
pp. 2274-2276 ◽  
Author(s):  
Romy Weller ◽  
Daniel Todt ◽  
Michael Engelmann ◽  
Martina Friesland ◽  
Heiner Wedemeyer ◽  
...  
2018 ◽  
Vol 154 (3) ◽  
pp. 663-674.e7 ◽  
Author(s):  
Xianfang Wu ◽  
Viet Loan Dao Thi ◽  
Peng Liu ◽  
Constantin N. Takacs ◽  
Kuanhui Xiang ◽  
...  

2015 ◽  
Vol 120 ◽  
pp. 134-139 ◽  
Author(s):  
Yuchen Nan ◽  
Zexu Ma ◽  
Harilakshmi Kannan ◽  
David A. Stein ◽  
Patrick I. Iversen ◽  
...  

2016 ◽  
Vol 64 (2) ◽  
pp. S518
Author(s):  
L. Xu ◽  
W. Wang ◽  
X. Zhou ◽  
Y. Wang ◽  
Y. Yin ◽  
...  

2010 ◽  
Vol 92 (3) ◽  
pp. 572-581 ◽  
Author(s):  
S. P. K. Varma ◽  
A. Kumar ◽  
N. Kapur ◽  
H. Durgapal ◽  
S. K. Acharya ◽  
...  

2017 ◽  
Vol 66 (1) ◽  
pp. S471-S472
Author(s):  
C. Qu ◽  
W. Wang ◽  
L. Xu ◽  
Y. Yin ◽  
Q. Pan ◽  
...  

2021 ◽  
Author(s):  
Changbo Qu ◽  
Yang Li ◽  
Yunlong Li ◽  
Yihang Pan

Abstract Hepatitis E virus (HEV) infection is the leading cause of acute hepatitis worldwide. Mitochondrial antiviral signaling protein (MAVS)-mediated interferon (IFN) response plays a pivotal role in the hepatic antiviral immunity. However, little is known about the effects of overexpression of MAVS on HEV infection. Here, we studied the effects of FL-MAVS on HEV. We found that overexpression of FL-MAVS profoundly inhibited HEV replication. The overexpression of FL-MAVS is accompanied by the secretion of functional IFNs and transcriptional induction of interferon stimulated genes (ISGs). Furthermore, we showed that the anti-HEV effect of FL-MAVS is largely dependent of the JAK signaling activation.


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