IV Mutation Detail Information

Virus Mutation IV Mutation E684G


Basic Characteristics of Mutations
Mutation Site E684G
Mutation Site Sentence The PR8-PA(0028)-E684G mutant showed significantly higher viral replication in mammalian cells as compared to PR8-PA(0028) and led to 100% mortality in mice, with significantly increased interferon beta expression.
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region PA
Standardized Encoding Gene PA
Genotype/Subtype -
Viral Reference -
Functional Impact and Mechanisms
Disease Influenza A    
Immune -
Target Gene -
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location Puerto Rico
Literature Information
PMID 29981696
Title Novel mutations in avian PA in combination with an adaptive mutation in PR8 NP exacerbate the virulence of PR8-derived recombinant influenza A viruses in mice
Author Lee CY,An SH,Kim I,Choi JG,Lee YJ,Kim JH,Kwon HJ
Journal Veterinary microbiology
Journal Info 2018 Jul;221:114-121
Abstract The polymerase complex of the low-pathogenic avian influenza virus [A/chicken/Korea/KBNP-0028/2000] (0028) has previously been characterized, and novel amino acid residues present in the polymerase acidic protein (PA) that likely contribute to pathogenicity toward mammals have been identified. In the present study, our aims were to generate A/Puerto Rico/8/34 (PR8)-derived recombinant viruses containing the 0028-PA gene with a single amino acid mutation and to test their pathogenicity and replication ability. We found that the recombinant viruses acquired additional single mutations in the nucleoprotein (NP). Because the additional mutations in NP did not affect viral pathogenicity, but rather attenuated viral replication and polymerase activity, the incompatibility of the avian PA gene within the PR8 backbone may have induced an adaptive mutation in NP. To minimize the differences due to NP mutations, we generated 0028-PA mutants with an E375G mutation, not affecting viral replication and pathogenicity, in the NP gene. The PR8-PA(0028)-E684G mutant showed significantly higher viral replication in mammalian cells as compared to PR8-PA(0028) and led to 100% mortality in mice, with significantly increased interferon beta expression. Thus, the E684G mutation in the PA gene may play an important role in viral pathogenicity in mice by increasing viral replication and the host immune response.
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.