Origin and molecular characterization of the human-infecting H6N1 influenza virus in Taiwan.
10.1007/s13238-013-3083-0
- Author:
Weifeng SHI
1
;
Yi SHI
;
Ying WU
;
Di LIU
;
George F GAO
Author Information
1. School of Medical Sciences, Taishan Medical College, Taian, 271016, China.
- Publication Type:Journal Article
- MeSH:
Amino Acid Sequence;
Amino Acid Substitution;
Animals;
Hemagglutinin Glycoproteins, Influenza Virus;
chemistry;
genetics;
Humans;
Influenza A Virus, H5N2 Subtype;
genetics;
physiology;
Influenza A virus;
genetics;
isolation & purification;
physiology;
Influenza, Human;
epidemiology;
virology;
Laboratories;
Models, Molecular;
Molecular Sequence Data;
Phylogeny;
Poultry;
virology;
Protein Conformation;
Taiwan;
epidemiology;
Viral Proteins;
genetics
- From:
Protein & Cell
2013;4(11):846-853
- CountryChina
- Language:English
-
Abstract:
In June 2013, the first human H6N1 influenza virus infection was confirmed in Taiwan. However, the origin and molecular characterization of this virus, A/Taiwan/2/2013 (H6N1), have not been well studied thus far. In the present report, we performed phylogenetic and coalescent analyses of this virus and compared its molecular profile/characteristics with other closely related strains. Molecular characterization of H6N1 revealed that it is a typical avian influenza virus of low pathogenicity, which might not replicate and propagate well in the upper airway in mammals. Phylogenetic analysis revealed that the virus clusters with A/chicken/Taiwan/A2837/2013 (H6N1) in seven genes, except PB1. For the PB1 gene, A/Taiwan/2/2013 was clustered with a different H6N1 lineage from A/chicken/Taiwan/ A2837/2013. Although a previous study demonstrated that the PB2, PA, and M genes of A/Taiwan/2/2013 might be derived from the H5N2 viruses, coalescent analyses revealed that these H5N2 viruses were derived from more recent strains than that of the ancestor of A/Taiwan/2/2013. Therefore, we propose that A/Taiwan/2/2013 is a reassortant from different H6N1 lineages circulating in chickens in Taiwan. Furthermore, compared to avian isolates, a single P186L (H3 numbering) substitution in the hemagglutinin H6 of the human isolate might increase the mammalian receptor binding and, hence, this strain's pathogenicity in humans. Overall, human infection with this virus seems an accidental event and is unlikely to cause an influenza pandemic. However, its co-circulation and potential reassortment with other influenza subtypes are still worthy of attention.
