IV Mutation Detail Information

Virus Mutation IV Mutation K88R


Basic Characteristics of Mutations
Mutation Site K88R
Mutation Site Sentence Based on previously identified candidate amino acids, we generated mutant 01310 PB2 genes with single amino acid mutations [PB2(01310)-I66M, PB2(01310)- K88R, PB2(01310)-I109V, PB2(01310)-I133V, PB2(01310)-R157K, PB2(01310)-K340R, PB2(01310)-L373I, PB2(01310)-V575M, PB2(01310)-E627K, and PB2(01310)-A674T] and tested their polymerase activity using an in vitro mini-genome assay in the 293T human embryonic kidney cell line (Fig. 1a).
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region PB2
Standardized Encoding Gene PB2
Genotype/Subtype H1N1
Viral Reference -
Functional Impact and Mechanisms
Disease Influenza A    
Immune -
Target Gene -
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location Korea
Literature Information
PMID 28860593
Title Prerequisites for the acquisition of mammalian pathogenicity by influenza A virus with a prototypic avian PB2 gene
Author Lee CY,An SH,Kim I,Go DM,Kim DY,Choi JG,Lee YJ,Kim JH,Kwon HJ
Journal Scientific reports
Journal Info 2017 Aug 31;7(1):10205
Abstract The polymerase of avian influenza A virus (AIV) is a heterotrimer composed of PB2, PB1, and PA. PB2 plays a role in overcoming the host barrier; however, the genetic prerequisites for avian PB2 to acquire mammalian pathogenic mutations have not been well elucidated. Previously, we identified a prototypic avian PB2 that conferred non-replicative and non-pathogenic traits to a PR8-derived recombinant virus when it was used to infect mice. Here, we demonstrated that key amino acid mutations (I66M, I109V, and I133V, collectively referred to as MVV) of this prototypic avian PB2 increase the replication efficiency of recombinant PR8 virus carrying the mutated PB2 in both avian and mammalian hosts. The MVV mutations caused no weight loss in mice, but they did allow replication in infected lungs, and the viruses acquired fatal mammalian pathogenic mutations such as Q591R/K, E627K, or D701N in the infected lungs. The MVV mutations are located at the interfaces of the trimer and are predicted to increase the strength of this structure. Thus, gaining MVV mutations might be the first step for AIV to acquire mammalian pathogenicity. These results provide new insights into the evolution of AIV in birds and mammals.
Sequence Data -
Mutation Information
Note
Basic Characteristics of Mutations
  • Mutation Site: The specific location in a gene or protein sequence where a change occurs.
  • Mutation Level: The level at which a mutation occurs, including the nucleotide or amino acid level.
  • Mutation Type: The nature of the mutation, such as missense mutation, nonsense mutation, synonymous mutation, etc.
  • Gene/Protein/Region: Refers to the specific region of the virus where the mutation occurs. Including viral genes, viral proteins, or a specific viral genome region. If the article does not specifically indicate the relationship between the mutation and its correspondence, the main
  • Gene/Protein/Region studied in the article is marked.
  • Genotype/Subtype: Refers to the viral genotype or subtype where the mutation occurs. If the article does not specifically indicate the relationship between the mutation and its correspondence, the main Genotype/Subtype studied in the article is marked.
  • Viral Reference: Refers to the standard virus strain used to compare and analyze viral sequences.
Functional Impact and Mechanisms
  • Disease: An abnormal physiological state with specific symptoms and signs caused by viral infection.
  • Immune: The article focuses on the study of mutations and immune.
  • Target Gene: Host genes that viral mutations may affect.
Clinical and Epidemiological Correlations
  • Clinical Information: The study is a clinical or epidemiological study and provides basic information about the population.
  • Treatment: The study mentioned a certain treatment method, such as drug resistance caused by mutations. If the study does not specifically indicate the relationship between mutations and their correspondence treatment, the main treatment studied in the article is marked.
  • Location: The source of the research data.
Literature Information
  • Sequence Data: The study provides the data accession number.