literature

IV mutation literature information.

In silico thermodynamic stability of mammalian adaptation and virulence determinants in polymerase complex proteins of H9N2 virus.

PMID: 30733797 2018 Journal, genetic engineering & biotechnology

Result: 391E, K318R, A661T, I504V and K526R were recognized in all viruses under study (Table 3).

Potential Pandemic of H7N9 Avian Influenza A Virus in Human.

PMID: 30533399 2018 Frontiers in cellular and infection microbiology

Abstract: Among the six internal viral genes, amino acid changes do not differ significantly between H9N2 and H7N9, except for V100A in PA, and K526R, D627K, and D701N in PB2.

Result: In comparisons of H7N9 and H9N2, the former has high proportions of the amino acid changes V100A in PA and K526R, E/D627K/N, and D701N in PB2.

Result: In waves 1-4, Q222L in HA and K526R in PB2 had high proportions in bo

Multiple polymerase gene mutations for human adaptation occurring in Asian H5N1 influenza virus clinical isolates.

PMID: 30166556 2018 Scientific reports

Introduction: Other mutations in PB2, PB1 and PA also influence the host range of influenza viruses; e.g., PB2-D701N, PB2-K526R, PB2-Q591K, PB2-E192K and -K702R, PB2-I147T/K399T/A588T, PB2-E158G, PB1-L13P/S678N, PB1-

Dynamic Variation and Reversion in the Signature Amino Acids of H7N9 Virus During Human Infection.

PMID: 29688498 2018 The Journal of infectious diseases

8Discussion: Our study also detected the PB2 K526R mutation (a ""functionally equivalent"" mutation) in cases 1 and 2, in whom the viruses lacked PB2 627K (Table 2)."

Result: Among other signature amino acids in the PB2 segment, the L89V and A588V mutations were detected in all the samples (Supplementary Table 1), while K526R substitutions occurred in 3 patients (Table 2).

Table: K526R

Novel Polymerase Gene Mutations for Human Adaptation in Clinical Isolates of Avian H5N1 Influenza Viruses.

PMID: 27097026 2016 PLoS pathogens

Introduction: However, a recent study showed that PB2-K526R, particularly in combination with PB2-627K, enhanced replication of certain influenza virus subtypes.

Introduction: Moreover, the PB2-D701N, PB2-Q591K, PB2-K526R, PB2-G590S/Q591R and PB2-I147T/K399T/A588T mutations increase influenza virus replication in mammalian hosts.

Genomic Signatures for Avian H7N9 Viruses Adapting to Humans.

PMID: 26845764 2016 PloS one

Result: Although S286G, R340K, M473V, K526R, T569A, and A588V were observed (Table 3), their association with K627E was seen in four or fewer instances.

PB2-588 V promotes the mammalian adaptation of H10N8, H7N9 and H9N2 avian influenza viruses.

PMID: 26782141 2016 Scientific reports

Discussion: Many adaptive mutations in PB2, such as E627K, D701N, K526R, and T271A have been proven to be important for different avian influenza viruses to break the host species barrier to infect mammals.

Deep sequencing of the transcriptome from murine lung infected with H5N8 subtype avian influenza virus with combined substitutions I283M and K526R in PB2 gene.

PMID: 25409547 2014 Nature communications

Abstract: PB2-K526R interacts with nuclear export protein and our results suggest that it contributes to enhance replication for certain influenza virus subtypes, particularly in combination with 627K.

Abstract: Here we show that mutation PB2-K526R is present in some human H7N9 influenza isolates, in nearly 80% of H5N1 human isolates from Indonesia and, in conjunction with E627K, in almost all seasonal H3N2 viruses since 1970.

Introduction: Various PB2 adaptation markers are identified among the H7N9 human isolates, and a K526R substitution associated with other previously defined adaptive markers is detected in some human isolates.

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