Partial glycosylation of the Ibaraki virus NS3 protein is sufficient to support virus propagation

Ibaraki virus (IBAV) causes Ibaraki disease. We have previously shown that IBAV NS3 protein is highly glycosylated and that tunicamycin, an inhibitor of N-linked glycosylation, suppressed NS3 glycosylation and viral propagation. Since tunicamycin is known to cause endoplasmic reticulum (ER) stress,...

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Bibliographic Details
Published in:Virology (New York, N.Y.) N.Y.), 2021-11, Vol.563, p.44-49
Main Authors: Maeda, Yuki, Shibutani, Shusaku, Iwata, Hiroyuki
Format: Article
Language:English
Subjects:
Animals
Cricetinae
Endoplasmic Reticulum Stress
ER stress
Gene Expression Regulation, Viral - drug effects
Gene Expression Regulation, Viral - physiology
Glycosylation
Ibaraki virus
NS3
Orbivirus
Orbivirus - genetics
Orbivirus - metabolism
Thapsigargin - pharmacology
Tunicamycin - pharmacology
Viral Nonstructural Proteins - genetics
Viral Nonstructural Proteins - metabolism
Virus Replication - physiology
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Description
Summary:Ibaraki virus (IBAV) causes Ibaraki disease. We have previously shown that IBAV NS3 protein is highly glycosylated and that tunicamycin, an inhibitor of N-linked glycosylation, suppressed NS3 glycosylation and viral propagation. Since tunicamycin is known to cause endoplasmic reticulum (ER) stress, we explored the effects of ER stress and NS3 glycosylation on IBAV infection using tunicamycin and thapsigargin. These reagents both induced ER stress and NS3 glycosylation inhibition in a concentration-dependent manner, and as in our previous report, high concentrations of tunicamycin and thapsigargin suppressed IBAV propagation. However, lower concentrations of these reagents produced limited differences in IBAV propagation, despite their ability to suppress NS3 glycosylation and induce ER stress. These findings suggest that a considerable degree of NS3 glycosylation inhibition and ER stress induction does not suppress IBAV propagation. Conversely, lower concentrations of thapsigargin enhanced IBAV propagation, suggesting that moderate ER stress could benefit IBAV. •Ibaraki virus (IBAV) propagation is suppressed by high concentrations of tunicamycin and thapsigargin.•Lower concentrations of tunicamycin and thapsigargin do not severely affect IBAV propagation.•Full glycosylation of the IBAV protein NS3 is not essential for propagation.•Moderate ER stress may promote IBAV propagation.
ISSN:0042-6822
1096-0341
DOI:10.1016/j.virol.2021.08.003