A Serine12Stop mutation in PB1-F2 of the 2009 pandemic (H1N1) influenza A: a possible reason for its enhanced transmission and pathogenicity to humans.
10.4142/jvs.2009.10.4.349
- Author:
Muthannan A RAMAKRISHNAN
1
;
Marie R GRAMER
;
Sagar M GOYAL
;
Srinand SREEVATSAN
Author Information
1. Veterinary Population Medicine Department, College of Veterinary Medicine, University of Minnesota, St. Paul, MN 55108, USA. sreev001@umn.edu
- Publication Type:Brief Communication ; Research Support, N.I.H., Extramural
- Keywords:
pandemic influenza A;
PB1-F2 protein;
S12Stop;
virulence marker
- MeSH:
Amino Acid Sequence;
Gene Expression Regulation, Viral/physiology;
Host-Pathogen Interactions;
Humans;
Influenza A Virus, H1N1 Subtype/*genetics/*pathogenicity;
Influenza, Human/*virology;
Molecular Sequence Data;
Mutation;
Viral Proteins/chemistry/*genetics/metabolism;
Virulence
- From:Journal of Veterinary Science
2009;10(4):349-351
- CountryRepublic of Korea
- Language:English
-
Abstract:
As the scientific community scrambles to define the ancestry and lineages of the eight segments of new pandemic H1N1 strain, we looked for unique genetic events in this virus's genome to explain the newly found enhanced virulence and transmissibility among humans. Genome annotations of this virus identified a stop mutation replacing serine at codon 12 (S12Stop) of the PB1-F2 protein, a virulence factor in influenza A viruses. Here, we discuss the significance of this finding and how it may contribute to host specialization, explaining the virtual absence of the H1N1 influenza A virus strain in pig populations. This finding is expected to lead to a better understanding of the transmission and pathogenesis of the 2009 pandemic strain.
