AVM v1, released 02-OCT-22

A manually curated database of aerosol-transmitted virus mutations, human diseases, and drugs

Mutation detail:


Mutation site K229R
Virus Influenzavirus A H1N1
Mutation level Amino acid Level
Gene/protein/region type PB1
Gene ID 23308122
Country UK
Mutation type nonsynonymous mutation
Genotype/subtype/clade -
Sample Human
Variants -
Viral reference sequence GQ166655.1
Drug/antibody/vaccine favipiravir resistant
Transmissibility -
Transmission mechanism -
Pathogenicity -
Pathogenicity mechanism -
Immune escape mutation -
Immune escape mechanism -
RT-PCR primers probes -

Protein detail:


Protein name Polymerase PB1
Uniprot protein ID C3W5X7
Protein length 757 amino acids
Protein description RNA-dependent RNA polymerase which is responsible for replication and transcription of virus RNA segments. The transcription of viral mRNAs occurs by a unique mechanism called cap-snatching. 5' methylated caps of cellular mRNAs are cleaved after 10-13 nucleotides by PA. In turn, these short capped RNAs are used as primers by PB1 for transcription of viral mRNAs. During virus replication, PB1 initiates RNA synthesis and copy vRNA into complementary RNA (cRNA) which in turn serves as a template for the production of more vRNAs

Literature information:


Pubmed ID 30352857
Clinical information No
Disease -
Published year 2018
Journal Proc Natl Acad Sci U S A
Title The mechanism of resistance to favipiravir in influenza
Author Daniel H Goldhill,Aartjan J W Te Velthuis,Robert A Fletcher,Pinky Langat,Maria Zambon
Evidence We demonstrate that a K229R mutation in motif F of the PB1 subunit of the influenza virus RNA-dependent RNA polymerase (RdRP) confers resistance to favipiravir in vitro and in cell culture.