AVM v1, released 02-OCT-22

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

Mutation detail:


Mutation site I42V
Virus Human rhinovirus
Mutation level Amino acid level
Gene/protein/region type P3-A
Gene ID 1461213
Country -
Mutation type nonsynonymous mutation
Genotype/subtype/clade B
Sample cell line
Variants -
Viral reference sequence NC_001490.1
Drug/antibody/vaccine aminothiazole resistant
Transmissibility -
Transmission mechanism -
Pathogenicity -
Pathogenicity mechanism -
Immune escape mutation -
Immune escape mechanism -
RT-PCR primers probes -

Protein detail:


Protein name 3A (P3-A)
Uniprot protein ID P03303
Protein length 85 amino acids
Protein description P3-A localizes the viral replication complex to the surface of membranous vesicles. It inhibits host cell endoplasmic reticulum-to-Golgi apparatus transport and causes the disassembly of the Golgi complex, possibly through GBF1 interaction. This would result in depletion of MHC, trail receptors and IFN receptors at the host cell surface. P3-A plays an essential role in viral RNA replication by recruiting ACBD3 and PI4KB at the viral replication sites, thereby allowing the formation of the rearranged membranous structures where viral replication takes place.

Literature information:


Pubmed ID 23650168
Clinical information No
Disease COPD(Chronic Obstructive Pulmonary Disorder)
Published year 2013
Journal Antimicrob Agents Chemother
Title Phosphatidylinositol 4-kinase III beta is essential for replication of human rhinovirus and its inhibition causes a lethal phenotype in vivo
Author Catherine Spickler,Julie Lippens,Marie-Kristine Laberge,Sophie Desmeules,Edith Bellavance
Evidence In vitro selection and sequencing of aminothiazole series-resistant HRV variants revealed a single-nucleotide mutation leading to the amino acid change I42V in the essential HRV 3A protein.