Neddylation of M1 negatively regulates the replication of influenza A virus.
PMID: 33016861
2020
The Journal of general virology
Abstract: However, we found that NEDD8 overexpression can still inhibit the replication of PB2 K699R mutant viruses, implying that other viral protein(s) can be neddylated.
Abstract: In addition, we found that the neddylation-deficient M1 mutant (M1 K187R) had a longer half-life than that of wild-type M1, indicating that the neddylation of M1 reduces stability.
Abstract: More importantly, we observed that overexpression of NEDD8 inhibited the replication of the wild-type WSN more effectively than that of WSN-M1 K187R.
Abstract: The data showed that the replication of WSN-M1 K
Structure-Based Modification of an Anti-neuraminidase Human Antibody Restores Protection Efficacy against the Drifted Influenza Virus.
Abstract: Furthermore, Z2B3-D102R can protect mice from A/Serbia/NS-601/2014 H1N1 virus (NA contains E432) infection while the wild-type Z2B3 antibody shows no protection.
Abstract: Here, we investigate a monoclonal antibody, Z2B3, isolated from an H7N9-infected patient, that exhibited cross-reactivity to both N9 (group 2) and a broad range of seasonal and avian N1 (group 1) proteins but lost activity to the N1 with the substitution K432E.
Abstract: It shows cross-reactivity to both group 1 (N1) and group 2 (N9) neuraminidases (NAs) but is sensitive to N1 NA with a K432E substitution.
Abstract: Structure-based modification o
PA Mutations Inherited during Viral Evolution Act Cooperatively To Increase Replication of Contemporary H5N1 Influenza Virus with an Expanded Host Range.
Result: Ancestral D1/PA-wt and the EG13G18E/R388S/E448A reverse mutant caused only a limited inflammatory response in the lungs of infected mice.
Result: As with most clade 2.2.1 viruses, both the EG13 and D1 viruses carry the PB2-E627K mutation.
Result: Based on the effects of the single mutations, we selected three PA substitutions (i.e.,
Figure: (A and C) Transparent surface diagrams of the D1/PA polymerase complex composed of PB2 (blue), PB1 (pink), and PA (green) with the A448E, S388R, and E18G mutations (red).
In Vitro Profiling of Laninamivir-Resistant Substitutions in N3 to N9 Avian Influenza Virus Neuraminidase Subtypes and Their Association with In Vivo Susceptibility.
Abstract: Both ma81K-N3R292K and ma81K-N8Q136K virus-infected mice exhibited reduced weight loss, mortality, and lung viral titers when treated with their susceptible NAIs, confirming the in vitro susceptibility of these substitutions.
Abstract: To determine whether the in vitro susceptibility of multi-NAI-resistant AIVs is associated with in vivo susceptibility, we infected BALB/c mice with recombinant AIVs with R292K (ma81K-N3R292K) or Q136K (ma81K-N8Q136K) NA substitutions, which impart in vitro susceptibility only to LAN or OS, respectively.
Detection and discrimination of influenza B Victoria lineage deletion variant viruses by real-time RT-PCR.
Abstract: There are currently five antigenically distinct HA proteins expressed by co-circulating influenza B viruses: B/YAM, B/VIC V1A (no deletion), B/VIC V1A-2DEL (2 aa deletion) and two antigenically distinguishable groups of B/VIC V1A-3DEL (3 aa deletion).
Abstract: We used propagated influenza B/VIC variant viruses and clinical specimens to assess assay performance.ResultsThis rRT-PCR assay detects and distinguishes the influenza B/VIC V1A, B/VIC V1A-2DEL, and B/VIC V1A-3DEL variant viruses, with no cross-reactivity.
Introduction: Sequencing analysis confirmed that these viruses have a deletion of 6 nucleotides (nt) in the haemagglutinin (HA) gene resulting in a 2 amino acid
Viral Subpopulation Screening Guides in Designing a High Interferon-Inducing Live Attenuated Influenza Vaccine by Targeting Rare Mutations in NS1 and PB2 Proteins.
Abstract: The PB2-D309N substitution enhanced the early transcription of interferon mRNA, revealing a novel role for the 309D residue in suppression of interferon responses.
Abstract: The enhanced interferon-inducing phenotypes were linked to either a deletion in NS1 (NS1Delta76-86) or a substitution in polymerase basic 2 protein (PB2-D309N).
The N-terminal residual arginine(19) of influenza A virus NS1 protein is required for its nuclear localization and RNA binding.
Abstract: Biological analysis of the rescued viruses indicated that the R19A mutation of NS1 did not interfere the replication of H5N1 virus during infection and attenuated the virulence of H5N1 virus in mice.
A Mutated PB1 Residue 319 Synergizes with the PB2 N265S Mutation of the Live Attenuated Influenza Vaccine to Convey Temperature Sensitivity.
Abstract: Furthermore, we show that the combined PB1 L319Q and PB2 N265S mutations confer temperature sensitivity on IAV polymerase activity in two different genetic backgrounds, PR8 and A/Cal/04/09.
Abstract: Here, we describe the origin/discovery of this unique mutation and demonstrate that, when combined with the PB2 N265S mutation of LAIV, it conveys an even greater level of temperature sensitivity and attenuation on PR8 than the complete set of attenuating mutations from LAIV.
Variability of nonpathogenic influenza virus H5N3 under immune pressure.
Abstract: Additionally, mutation S145P increased the temperature of HA heat inactivation, compared to wild-type, as was proved by reverse genetics.
Genetic sequencing of influenza A (H1N1) pdm09 isolates from South India, collected between 2011 and 2015 to detect mutations affecting virulence and resistance to oseltamivir.
PMID: 33154243
2020
Indian journal of medical microbiology
Abstract: All the study isolates possessed H274 residue and 7 strains had N295S, the next most common mutation found in oseltamivir-resistant variants.
Abstract: Conclusion: In this study, although H274Y mutation associated with oseltamivir resistance has not been noted, significant mutations have been noted in both HA and NA genes including D239N, N295S, V106I, Q136K, N248D, V267A.
Abstract: Two samples collected from expired patients had D239N (D222G or D225G) mutation in HA.
IV mutation literature information.
PMID: 
2020
The Journal of general virology
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