Abstract
BackgroundHighly pathogenic avian influenza (HPAI) H5N1 viruses continue to circulate in poultry and can infect and cause mortality in birds and mammals; the genetic determinants of their increased virulence are largely unknown. The main purpose of this work was to determine the correlation between known molecular determinants of virulence in different avian influenza virus (AIV) genes and the results of experimental infection of birds and mammals with AIV strain A/swan/Mangistau/3/06 (H5N1; SW/3/06).Methods and resultsWe examined the virulence of SW/3/06 in four species of birds (chickens, ducks, turkeys, geese) and five species of mammals (mice, guinea pigs, cats, dogs, pigs), and identified the molecular determinants of virulence in 11 genes (HA, NA, PB1, PB1-F2, PB2, PA, NS1, NS2, M1, M2 and NP). SW/3/06 does not possess the prime virulence determinant of HPAIV – a polybasic HA cleavage site – and is highly pathogenic in chickens. SW/3/06 replicated efficiently in chickens, ducks, turkeys, mice and dogs, causing 100% mortality within 1.6–5.2 days. In addition, no mortalities were observed in geese, guinea pigs, cats and pigs. The HI assay demonstrated all not diseased animals infected with the SW/3/06 virus had undergone seroconversion by 14, 21 and 28 dpi. Eleven mutations in the seven genes were present in SW/3/06. These mutations may play a role in the pathogenicity of this strain in chickens, ducks, turkeys, mice and dogs. Together or separately, mutations 228S-103S-318I in HA may play a role in the efficient replication of SW/3/06 in mammals (mice, dogs, pigs).ConclusionsThis study provides new information on the pathogenicity of the newly-isolated swan derived H5N1 virus in birds and mammals, and explored the role of molecular determinants of virulence in different genes; such studies may help to identify key virulence or adaptation markers that can be used for global surveillance of viruses threatening to emerge into the human population.Electronic supplementary materialThe online version of this article (doi:10.1186/s12985-014-0207-y) contains supplementary material, which is available to authorized users.
Highlights
Pathogenic avian influenza (HPAI) H5N1 viruses continue to circulate in poultry and can infect and cause mortality in birds and mammals; the genetic determinants of their increased virulence are largely unknown
This study provides new information on the pathogenicity of the newly-isolated swan derived H5N1 virus in birds and mammals, and explored the role of molecular determinants of virulence in different genes; such studies may help to identify key virulence or adaptation markers that can be used for global surveillance of viruses threatening to emerge into the human population
The present study examined the correlation between known and novel molecular determinants of virulence in influenza genes with the results of experimental infection of birds and mammals with the avian influenza virus (AIV) strain A/ swan/Mangistau/3/06 (H5N1; SW/3/06) that was isolated in 2006 from a dead swan found in the Mangistau region of the Republic of Kazakhstan
Summary
Pathogenic avian influenza (HPAI) H5N1 viruses continue to circulate in poultry and can infect and cause mortality in birds and mammals; the genetic determinants of their increased virulence are largely unknown. Influenza A viruses have eight-segmented, negative, singlestranded RNA genomes and are serologically divided into 18 hemagglutinin (HA, H1-H18) and eleven neuraminidase (NA, N1-N11) subtypes [1,2]. Viruses typically acquire critical alterations in their genomes that allow them to adapt to or severely damage their host. Identification of these genetic changes will improve our understanding of the determinants of virulence and aid in the development of counter measures against viral infection and spread [6]. A number of genetic determinants are associated with the virulence and ability of avian influenza viruses (AIVs) to replicate in mammalian cells [7]. The switch in host cell receptor specificity from sialic acid connected to galactose via α2-3 linkages (avian) to α2-6
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