Abstract: Mutations were found in HA (A135 T, T136S, and T160 A [H3 numbering]), M1 (N30D and T215 A), NS1 (P42S and D97 E), PB2 (R389 K), and PA (N383D) proteins; these mutations have been shown to be related to mammalian adaptation and changes in virulence of AIVs.
Discussion: In this study, no key amino acid mutations were found in PB2, especially the E627 K and D701 N mutations, which have b
Mutations during the adaptation of H7N9 avian influenza virus to mice lungs enhance human-like sialic acid binding activity and virulence in mice.
Abstract: Sequence analysis showed that the two viruses differed by 27 amino acids distributed among six genes, containing changes in PB2 (E627K, D701N) and HA (Q226L) genes.
Can molecular dynamics explain decreased pathogenicity in mutant camphecene-resistant influenza virus?
PMID: 33480324
2021
Journal of biomolecular structure & dynamics
Abstract: Specifically, camphecene causes a significant mutation in HA (V615L).
Identification of Important N-Linked Glycosylation Sites in the Hemagglutinin Protein and Their Functional Impact on DC-SIGN Mediated Avian Influenza H5N1 Infection.
PMID: 33451024
2021
International journal of molecular sciences
Abstract: Furthermore, combined mutations (N27Q&N39Q) significantly waned the interaction on either H5N1-PVs or -RG infection in cis and in trans (p < 0.01).
Abstract: Human recombinant DC-SIGN (rDC-SIGN) coated ELISA showed that H5N1-PVs bound to DC-SIGN, however, mutation on the N27Q, N39Q, and Method: The pHW1203-HA with different N-linked glycosylation mutations including N26Q, N27Q, N39Q, N170Q, N181Q, N209Q, N302Q, N500Q, N599Q and other combination of mutations were generated.
N-linked glycosylation at site 158 of the HA protein of H5N6 highly pathogenic avian influenza virus is important for viral biological properties and host immune responses.
Abstract: We have shown earlier that lack of glycosylation at position 158 of the hemagglutinin (HA) glycoprotein due to the T160A mutation is a key determinant of the dual receptor binding property of clade 2.3.4.4 H5NX subtypes.
Introduction: Compared to the surface Hemagglutinin (HA
Result: We conducted a PCR-based site-directed mutagenesis to generate several viruses with a single amino acid change at 160, including T160A in RHX (RHX-160A) and A160T in RY6 (RY6-160T).
Discussion: reported that addition of an N158D mutation to an HA protein containing N224K/Q226L increases virus stability.
Identification of a Permissive Secondary Mutation That Restores the Enzymatic Activity of Oseltamivir Resistance Mutation H275Y.
Abstract: Here, we studied two new potential adaptive mutations, V292I and D740A, in the PB2 protein that were identified by a multi-factor regression model.
Abstract: The study shows that the prevalence of the PB2-V292I mutation is increased in H7N9 influenza viruses isolated from both humans and birds over the past 6 years.
Identification of a Permissive Secondary Mutation That Restores the Enzymatic Activity of Oseltamivir Resistance Mutation H275Y.
PMID: 33309772
2021
Infection, genetics and evolution
Abstract: Especially, PB2-I283M-K526R mutation strongly induced a sharp expression of cytokine storm-related genes, including MX1, CXCL10, and IFN-gamma, performed by qRT-PCR.
Abstract: Here, RNA-seq method was used to analyze the global host response of murine lungs after infecting with parental r-JY virus and JY-PB2-I283M-K526R mutant virus.
Abstract: Taken together, our data demonstrated that PB2-I283M-K526R of H5N8 subtype HPAIV exacerbated the innate immune response and the level of cell apoptosis, which might be a key pathogenic mechanism for the enhanced pathogenicity of mutants in mammals.
Abstract: We also found that P
Identification of a Permissive Secondary Mutation That Restores the Enzymatic Activity of Oseltamivir Resistance Mutation H275Y.
Abstract: Electrophysiology and DFT studies also show that the complexes block the G34E amantadine-resistant mutant despite some crowding in the binding site by the glutamates.
Abstract: In voltage-clamp oocyte studies using the ubiquitous amantadine-insensitive M2 S31N variant, the current block showed fast and slow phases, in contrast to the single phase found for amantadine block of wild-type M2.
Comprehensive assessment of amino acid substitutions in the trimeric RNA polymerase complex of influenza A virus detected in clinical trials of baloxavir marboxil.
PMID: 33099886
2021
Influenza and other respiratory viruses
Abstract: RESULTS: PA/I38N in A(H1N1)pdm09 and PA/I38R in A(H3N2) were newly identified as treatment-emergent substitutions in the CAPSTONE-2 study.
Abstract: The I38N substitution conferred reduced susceptibility by 24-fold, whereas replicative capacity of the I38N-substituted virus was impaired compared with the wild-type.
Abstract: The I38R-substituted virus was not viable in cell culture.
Method: In the CAPSTONE-2 study, next-generation sequencing (NGS) was also employed with the samples meeting the following criteria: (a) subjects shedding A(H3N2) viruses with PA/I38T substitution, (b) virology data (viral titer and RNA) are available at days 1, 2, 3 or 4, and
Genetic and Molecular Characterization of H9N2 Avian Influenza Viruses Isolated from Live Poultry Markets in Hubei Province, Central China, 2013-2017.
Abstract: Molecular analysis demonstrated that six H9N2 isolates had additional potential glycosylation sites at position 218 in the hemagglutinin protein, and all isolates had I155T and Q226L mutations.
Abstract: Moreover, 44 strains had A558V mutations in the PB2 protein and four had E627V mutations, along with H9N2 human infection strains A/Beijing/1/2016 and A/Beijing/1/2017.
IV mutation literature information.
PMID: 
2021
Poultry science
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