Discussion: Some common variations of NS1 are amino-acid substitutions at particular sites (e.g., S42P, S42G, D92E, D92Y, I106M and A149V) that are responsible for virus growth, the ability to inhibit induction of IFN in vitro and in vivo, and viral pathogenesis in mice.
Major contribution of the RNA-binding domain of NS1 in the pathogenicity and replication potential of an avian H7N1 influenza virus in chickens.
Result: The kinetics of viral replication in the lung was slightly delayed with the A149V virus, for which the highest loads were observed at days 2 and 3 p.i.
Result: The latter observation could result from the fact that the effect of the A149V substitution was compensated for by the presence of the wt-RBD.
Result: The wt-virus, and to a slightly lesser extent the A149V-virus, were found in the kidneys and brains, indicating limited systemic dissemination.
Result: Transient expression of wt-
Discussion: Therefore, if we disregard these potentially biased observations, our data indicated that (i) the individually-expressed wt-RBD, but not its 3841AA mutant, induced a ~ 38% increase in the polymerase activity; (ii) the individually-expressed A149V-ED induced a ~ 30% increase in the polymerase activity; (iii) when adjoined.
Virulence of an H5N8 highly pathogenic avian influenza is enhanced by the amino acid substitutions PB2 E627K and HA A149V.
PMID: 28750900
2017
Infection, genetics and evolution
Abstract: Substitutions in the HA (A149V) and PB2 (E627K) proteins led to enhanced viral virulence in mice, the viruses displayed expanded tissue tropism, and increased replication kinetics in mammalian cells.
Abstract: The virulence of mouse-adapted virus was increased and adaptive mutations, HA (A149V) and PB2 (E627K), were detected after the ninth passage in each series of mice.
Highly pathogenic avian influenza virus H5N1 controls type I IFN induction in chicken macrophage HD-11 cells: a polygenic trait that involves NS1 and the polymerase complex.
Introduction: A recent study, for instance, reported that the highly pathogenic (HP) AIV A/goose/Guangdong/1/96 (H5N1) antagonized the induction of type I IFN in chicken embryo fibroblasts, whereas a recombinant virus carrying a valine instead of the alanine at position 149 of NS1 lost this function and became avirulent.
IV mutation literature information.
PMID: 
2018
Virology journal
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