literature

IV mutation literature information.

Highly pathogenic avian influenza H7N9 viruses with reduced susceptibility to neuraminidase inhibitors showed comparable replication capacity to their sensitive counterparts.

PMID: 31266524 2019 Virology journal

Method: NA K292R Forward, ccctgccaattgtccctgcatgtgcaggtaatc.

Method: NA K292R Reverse, gattacctgcacatgcagggacaattggcaggg.

A Single Amino Acid Substitution at Residue 218 of Hemagglutinin Improves the Growth of Influenza A(H7N9) Candidate Vaccine Viruses.

PMID: 31270231 2019 Journal of virology

Method: For rgGD17, the HA and NA genes from the highly pathogenic A/Guangdong/17SF003/2016 (GD17WT) were initially PCR amplified and cloned into cloning vector pGEM-T Easy (Promega, Madison, WI) for modification, with which we deleted the codon for the multibasic cleavage site RKRT from the HA gene and generated K292R (N2 numbering) mutation in NA to restore the neuraminidase inhibitor (NAi) sensitivity.

Result: Therefore, we generated the low-pathogenic A(H7N9) CVV rgGD17 from the HPAI GD17WT by removing the multibasic motif in HA and introducing K292R in

PMID: 12062393 2002 Antiviral research

Abstract: The predominant mutation seen is the substitution of arginine for lysine at position 292 of the viral NA.

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