N-benzyl 4,4-disubstituted piperidines as a potent class of influenza H1N1 virus inhibitors showing a novel mechanism of hemagglutinin fusion peptide interaction.
PMID: 32220685
2020
European journal of medicinal chemistry
Abstract: Furthermore, the HA1-S326V mutation resulting in resistance to 2 is close to the proposed new binding pocket.
Influenza vaccine effectiveness by A(H3N2) phylogenetic sub-cluster and prior vaccination history: 2016-17 and 2017-18 epidemics in Canada.
PMID: 32215564
2020
The Journal of infectious diseases
Abstract: Circulating 3C.2a viruses showed considerable diversity in the hemagglutinin glycoprotein and the egg-adapted vaccine strain also bore mutations, notably T160K loss-of-glycosylation.
Detection of H3N8 influenza A virus with multiple mammalian-adaptive mutations in a rescued Grey seal (Halichoerus grypus) pup.
Abstract: From examining the protein alignments, we found several residue changes in the seal virus that did not occur in the bird viruses, including D701N in the PB2 segment, a rare mutation, and a hallmark of mammalian adaptation of bird viruses.
Discussion: D701N is common in canine and horse H3N8 IAV (see Supplementary Table S4), but does not occur in birds, and was found associated with highly-pathogenic H5N1 viruses which infected humans.
Discussion: D701N mutation was also found in the A/harbor_seal/Massachusetts/1/2011, but not in the H10N7 outbreak, despite sustained transmission in seals for several months, nor in any other previously sequenced seal PB2 genes.
Discussion: This likely indicates adaptation to the seal environment, a hypothesis supported by the occurrence of the PMID: 32200160
2020
Research in veterinary science
Abstract: Genomic analysis of the mouse-adapted virus revealed amino acid changes in the PB2 (E525G, M645I, and D701N), NP (I475V), HA(D103N), and NA(K142E) proteins.
An R195K Mutation in the PA-X Protein Increases the Virulence and Transmission of Influenza A Virus in Mammalian Hosts.
Abstract: PA-X R195K was present in all human H7N9 and H1N1/2009 viruses and predominated in human H5N6 viruses.
Abstract: Reverse genetics analyses of PA-X substitutions conserved in human influenza viruses indicated that R195K, K206R, and P210L substitutions conferred significantly increased replication and pathogenicity on H9N2 virus in mice and ferrets.
Antigenic drift of hemagglutinin and neuraminidase in seasonal H1N1 influenza viruses from Saudi Arabia in 2014 to 2015.
Abstract: Amino acid changes at key antigenic sites, such as position S101N, S179N (antigenic site-Sa), I233T (antigenic site-Sb) in the head domain might have resulted in antigenic drift and emergence of variant viruses.
Abstract: For NA protein, 36% isolates showed the presence of amino acid changes such as V13I (n = 29), I314M (n = 29) and 12% had I34V (n = 10).
Abstract: However, H257Y mutation responsible for resistance to neuraminidase inhibitors was missing.
Introduction: Furthermore, a high number of the strains possessed the amino acid changes D97N (aspartic acid to asparagine), S185T
Antigenic changes among the predominantly circulating C/Sao Paulo lineage strains of influenza C virus in Yamagata, Japan, between 2015 and 2018.
PMID: 32135195
2020
Infection, genetics and evolution
Abstract: Aichi99 sublineage strains exhibiting decreased reactivity with the monoclonal antibody YA3 became predominant after 2016, and these strains possessed the K190N mutation.
Abstract: The Aichi99 sublineage strains possessing the K190N mutation were detected after 2012 in Europe, Australia, the USA, and Asia as well as Japan.
Abstract: These observations suggest that antigenic variants with K190N mutations have circulated extensively around the world and caused outbreaks in Japan between 2016 and 2018.
Contribution of Fc-dependent cell-mediated activity of a vestigial esterase-targeting antibody against H5N6 virus infection.
Figure: (C) Binding of human C1q to 9F4-K322A is abolished.
Figure: Balb/c mice were infected with 100 PFU of rgPR8 H5N6 and received a single therapeutic dose of 9F4-WT, 9F4-K322A or the isotype control 1A4 at 10 mg/kg via intraperitoneal injections 24 hpi.
Figure: ELISA was performed to compare the binding affinity of 9F4-WT with (A) 9F4-LALA or (B) 9F4-K322A to H5N6-HA.
Figure: Mouse FcgammaRIV-based ADCC reporter assay was performed for 9F4-WT, (A) 9F4-LALA and (B) 9F4-K322A as described in materials and methods.
Figure: Pseudotyped lentiviral particles harbouring the HA proteins of H5N6 IAV were incubated with 10-fold seriall
Figure: mFcgammaRIV activation is induced by 9F4-WT and 9F4-K322A but not 9F4-LALA.
Neuraminidase from Influenza A and B Viruses is Susceptible to the Compound 4-(4-Phenyl-1H-1,2,3-Triazol-1-yl)-2,2,6,6-Tetramethylpiperidine-1- Oxyl.
PMID: 31880262
2020
Current topics in medicinal chemistry
Abstract: When we passaged the influenza A virus in the presence of Tritempo, a mutant virus with the G248P change in the NA was detected.
X-ray Crystal Structures of the Influenza M2 Proton Channel Drug-Resistant V27A Mutant Bound to a Spiro-Adamantyl Amine Inhibitor Reveal the Mechanism of Adamantane Resistance.
1Abstract: Compared to the M2 ""wild type"" (WT) with valine at position 27, we observe that the channel pore is wider at its N-terminus as a result of the V27A mutation and that this removes V27 side chain hydrophobic interactions that are important for binding of amantad
Abstract: A 300 ns molecular dynamics simulation of the M2(22-46) V27A-spiro-adamantyl amine complex predicts with accuracy the position of the ligands and waters inside the pore in the X-ray crystal structure of the M2(22-46) V27A complex.
Abstract: Additionally, in the structure of the M2(21-61) V27A construct, the C-terminus of the channel is tightly packed relative to that of the M2(22-46) construct.
IV mutation literature information.
PMID: 
2020
European journal of medicinal chemistry
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