Introduction: For example, amino acid substitution G45R on the NS1 protein of A/Puerto Rico/8/1934 (H1N1) enhanced viral replication and increased virulence by inducing an earlier and robust proinflammatory cytokine response, while T49E mutation impairs its binding to TRIM25 and complex formation with RIG-I, thereby switching off its interferon antagonistic activity.
G45R on nonstructural protein 1 of influenza A virus contributes to virulence by increasing the expression of proinflammatory cytokines in mice.
Abstract: Microarray analysis revealed that A549 cells infected with the G45R/NS1 virus had higher expression of genes encoding proteins associated with the innate immune response and cytokine activity than cells inf
Abstract: Our findings suggest that G45R on NS1 protein contributes to viral virulence by increasing the expression of inflammatory cytokines early in infection.
Abstract: Replication of the G45R/NS1 virus was higher than that of the WT/NS1 virus in vitro, but the replication of both viruses was similar in mouse lungs.
Abstract: The G45R/NS1 virus had increased virulence by inducing an earlier and robust proinflammatory cytokine response in mice.
G45R on nonstructural protein 1 of influenza A virus contributes to virulence by increasing the expression of proinflammatory cytokines in mice.
Conclusion: As we have demonstrated that G45R/NS1 virus induced the type I IFN induction and response in infected A549 cells, it is also interesting to investigate virus virulence for further studies.
Figure: RIG-I mediated IFNbeta-promoter activity in 293 T cells expressing PR8 NS1 (wild type; WT, G45R and R38AK41A; AA), RIG I and IFNbeta-promoter luciferase reporter at 24 h post infection.
Figure: Replication kinetics of the rX31 virus encoding PR8 NS1s (WT, G45R or R38AK41A (AA)) in wild type (WT) and type I IFN receptor null (IFNARnull) Let1 cells.
Figure: b
Figure: rX31 virus with G45R NS1 also replicated to significantly high titer compared to the WT virus early in infection.
IV mutation literature information.
PMID: 
2018
Veterinary research
Browser Board
Co-occurred Entities
Filtrator
ViMRT