Immune Escape of Bovine Parvovirus by VP1 Inhibiting IFN-β Production
through RIG-I like Receptors Pathway
Abstract
Objective The present study aimed to explore if bovine parvovirus (BPV)
impacts beta interferon (IFN-β) production and to reveal further
molecular mechanism of BPV immune escape. Method The pCMV-Myc-BPV-VP1
recombinant plasmid was verified with both double enzyme digestion and
sequence. HEK 293T cells were transfected with this recombinant protein,
then infected with the vesicular stomatitis virus (VSV). Expression
levels of IFN-β mRNA were detected using qPCR. Results Expression level
of BPV VP1 mRNA in pCMV-Myc-BPV-VP1 group was significantly higher than
those of the untreated group (UT) and pCMV-Myc vector group. BPV virus
copies in bovine turbinate (BT) cells of BPV-VP1 group were raised
(P<0.05) with an increment of 5.8×104. Expression levels of
IFN-β mRNA of BPV VP1 group in HEK 293T cells were decreased
(P<0.01). Following treatment of TBK1 and IRF3(5D), IFN-β
expression levels in HEK 293T cells were depressed. Expression levels of
TBK1, IRF3(5D), MDA5 and MAVS were lower than those of their self
treatment. Conclusion pCMV-Myc-BPV-VP1 could heighten transcription
levels of VP1 protein in BT cells, promote BPV proliferation and ascend
the production of IFN-β. Overexpression of pCMV-Myc-BPV-VP decreased
IFN-β mRNA expression in HEK 293T cells and inhibited IFN-β production
induced by TBK1 and IRF3(5D). Furthermore, BPV VP1 obviously declined
expression levels of TBK1, IRF3(5D), MDA5 and MAVS in RLR pathway. Our
findings revealed a new mechanism evolved by BPV VP1 to inhibit type I
IFN production and provided a solid basis into the immunosuppression of
BPV, which is beneficial for developing novel strategy oftherapy of BPV
disease.