Key result
JIP4 exhibits antiviral properties against Influenza A virus by reducing viral polymerase activity, a function that is dynamically controlled by its phosphorylation at S730.
Why the study?
Influenza A virus infection is a world health concern with high treatment resistance rates, prompting investigation into host pathways modified in infection as promising new targets.
Does JIP4 phosphorylation at S730 reduce Influenza A virus replication in infected cells?
Does JIP4 phosphorylation at S730 reduce Influenza A virus replication in infected cells?
JIP4 exhibits antiviral properties against Influenza A virus by reducing viral polymerase activity, a function dynamically controlled by its phosphorylation at S730.
JIP4 modulation may guide host-directed IAV antivirals; leaves open in vivo efficacy and clinical translation.
Influenza A virus (IAV) infection is a world health concern, and current treatment options encounter high rates of resistance. Our group investigates host pathways modified in IAV infection as promising new targets. The host protein JIP4 is dynamically phosphorylated in IAV infection. JIP4 absence resulted in higher virus titers and viral protein and mRNA accumulation within the first replication cycle. Accordingly, decreased IAV titers and protein accumulation were observed during JIP4 overexpression. Strikingly, the antiviral function of JIP4 does not originate from modulation of JNK or p38 MAPK pathways or from altered expression of interferons or interferon-stimulated genes but rather originates from a reduction in viral polymerase activity. The interference of JIP4 with IAV replication is linked to the phosphorylation of serine 730. We provide evidence that JIP4, a host protein modulated in IAV infection, exhibits antiviral properties that are dynamically controlled by its phosphorylation at S730.
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Sarto et al. (2021) studied Influenza A Virus (IAV) infection. JIP4 modulation (silencing or overexpression) vs. Control (scrambled siRNA or empty vector) was evaluated on Viral replication (titers) and viral polymerase activity. JIP4 exhibits antiviral properties against Influenza A virus by reducing viral polymerase activity, a function that is dynamically controlled by its phosphorylation at S730.
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