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A Serine12Stop mutation in PB1-F2 of the 2009 pandemic (H1N1) influenza A: a possible reason for its enhanced transmission and pathogenicity to humans

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 vir...

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Detalles Bibliográficos
Autores principales: Ramakrishnan, Muthannan A., Gramer, Marie R., Goyal, Sagar M., Sreevatsan, Srinand
Formato: Texto
Lenguaje:English
Publicado: The Korean Society of Veterinary Science 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2807273/
https://www.ncbi.nlm.nih.gov/pubmed/19934602
http://dx.doi.org/10.4142/jvs.2009.10.4.349
Descripción
Sumario: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.