IV Mutation Detail Information

Virus Mutation IV Mutation F35L


Basic Characteristics of Mutations
Mutation Site F35L
Mutation Site Sentence HA D222G altered the receptor binding properties of the virus, and PA F35L increased its polymerase activity; the mutant virus was therefore similar to our G1 or HAmutPAmut strain.
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region HA
Standardized Encoding Gene HA
Genotype/Subtype H1N1
Viral Reference -
Functional Impact and Mechanisms
Disease Cell line    
Immune -
Target Gene -
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location -
Literature Information
PMID 22809692
Title Both influenza hemagglutinin and polymerase acidic genes are important for delayed pandemic 2009 H1N1 virus clearance in the ferret model
Author Ducatez MF,Ilyushina NA,Fabrizio TP,Rehg JE,Bovin NV,Webster RG,Webby RJ
Journal Virology
Journal Info 2012 Oct 25;432(2):389-93
Abstract We previously showed that a pandemic virus, A/Tennessee/560/09(H1N1), had the potential to adapt to human bronchial epithelial cells by the acquisition of hemagglutinin (HA) K154Q and polymerase acidic (PA) protein L295P mutations that conferred a more virulent phenotype. To better elucidate the role of each mutations, we generated recombinant viruses carrying single mutations or both mutations concurrently. The replication of all mutant viruses was significantly higher than that of the wild-type A/Tennessee/560/09 virus in human cells. The HA K154Q mutation reduced the receptor binding affinity of A/Tennessee/560/09 virus to 6-Su-6'SLN and biantennary 6'SLN receptors. In ferrets, H1N1 virus with HA K154Q and PA L295P mutations exhibited significantly higher titers in the upper respiratory tract compared to all other viruses 6 days post-infection. Our results suggest that both single mutations HA K154Q and PA L295P are necessary for delayed virus clearance of A/Tennessee/560/09(H1N1) influenza virus in a ferret animal model.
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.