We show here that NS1 protein from human H5N1 influenza isolate A/HK/156/97 reduces both systemic and pulmonary pro-inflammatory cytokines in an in vivo mouse model and protects against bone marrow lymphocyte depletion, an effect which has been shown to be mediated by TNFalpha.
We show here that NS1 protein from human H5N1 influenza isolate A/HK/156/97 reduces both systemic and pulmonary pro-inflammatory cytokines in an in vivo mouse model and protects against bone marrow lymphocyte depletion, an effect which has been shown to be mediated by TNFalpha.
We conclude that a well-regulated IFN response, with the ability to overcome early viral immune inhibition, without hyperinflammation, contributes to the ability of ducks to survive H5N1 influenza replication in their airways, and yet clear systemic infection and limit disease.
Moreover, duck AvIFIT binds to nucleoprotein (NP) of H5N1 influenza virus and upregulates the expression of genes involving the IFN pathway in DF1 cells.
Moreover, duck AvIFIT binds to nucleoprotein (NP) of H5N1 influenza virus and upregulates the expression of genes involving the IFN pathway in DF1 cells.
We conclude that a well-regulated IFN response, with the ability to overcome early viral immune inhibition, without hyperinflammation, contributes to the ability of ducks to survive H5N1 influenza replication in their airways, and yet clear systemic infection and limit disease.
In particular, activation of NF-kappaB is a bottleneck for the expression of IFN-beta and thus influences the expression of IFN-dependent genes indirectly in the primary innate immune response against H5N1 influenza virus.
In particular, activation of NF-kappaB is a bottleneck for the expression of IFN-beta and thus influences the expression of IFN-dependent genes indirectly in the primary innate immune response against H5N1 influenza virus.
Herein, we found that HIST1H1C expression, phosphorylation and methylation levels are decreased when infected with H1N1 influenza virus and increased when infected with H5N1 influenza virus.
Mice intranasally inoculated with saline or the HK483 virus were exposed to hypercapnia for 5 min at 0, 2, 4, or 6 dpi, followed by immunohistochemistry to determine the expression of nucleoprotein of H5N1 influenza A (NP) alone and coupled with 1) tyrosine hydroxylase (TH) in the carotid body and LC, 2) NK<sub>1</sub>R in the RTN, and 3) tryptophan hydroxylase (TPH) in the raphe.