Method: The H7N9 NS1 mutants, NS1 (R55E), NS1 (H63Q), NS1 (E70K), NS1 (P87S), NS1 (S114P), NS1 (A143T), NS1 (I178V) and NS1 (S212P) were generated by site-directed mutagenesis with the QuickChange XL system (Stratagene, La Jolla, CA, USA).
Result: The substitutions were the following (avian_residue/Position/human_residue): R55E,
PB2 segment promotes high-pathogenicity of H5N1 avian influenza viruses in mice.
Abstract: These include the independent emergence of HA A143T mutants, accumulation of four NA mutations, and farm-to-farm spread of virus variants harboring mammalian host determinants D701N and S714I in PB2.
Molecular determinants of adaptation of highly pathogenic avian influenza H7N7 viruses to efficient replication in the human host.
Abstract: These in vitro studies confirmed the roles of the E627K substitution in basic polymerase 2 (PB2) and the A143T substitution in HA in pathogenicity observed in a mouse model previously.
IV mutation literature information.
PMID: 
2018
Veterinary research
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