Molecular and phylogenetic analysis of matrix gene of avian influenza viruses isolated from wild birds and live bird markets in the USA
Article first published online: 8 SEP 2012
© 2012 John Wiley & Sons Ltd
Influenza and Other Respiratory Viruses
Volume 7, Issue 4, pages 513–520, July 2013
How to Cite
Chander, Y., Jindal, N., Sreevatsan, S., Stallknecht, D. E. and Goyal, S. M. (2013), Molecular and phylogenetic analysis of matrix gene of avian influenza viruses isolated from wild birds and live bird markets in the USA. Influenza and Other Respiratory Viruses, 7: 513–520. doi: 10.1111/irv.12003
- Issue published online: 11 JUN 2013
- Article first published online: 8 SEP 2012
- Accepted 24 July 2012. Published Online 8 September 2012.
- antiviral resistance;
- avian influenza virus;
- live bird markets;
- matrix gene;
- wild birds
Please cite this paper as: Chander et al. (2012) Molecular and phylogenetic analysis of matrix gene of avian influenza viruses isolated from wild birds and live bird markets in the USA. Influenza and Other Respiratory Viruses 7(4), 513–520.
Background Wild birds are the natural hosts for influenza A viruses (IAVs) and provide a niche for the maintenance of this virus.
Objectives This study was undertaken to analyze nucleotide sequences of the matrix (M) gene of AIVs isolated from wild birds and live bird markets (LBMs) to index the changes occurring in this gene.
Methods M-gene of 229 avian influenza virus (AIV) isolates obtained from wild birds and LBMs was amplified and sequenced. Full-length sequences (∼900 nt.) thus obtained were analyzed to identify changes that may be associated with resistance to adamantanes. Phylogenetic analysis of all sequences was performed using clustalw, and evolutionary distances were calculated by maximum composite likelihood method using mega (ver. 5.0) software.
Results Twenty-seven different viral subtypes were represented with H3N8 being the most dominant subtype in wild birds and H7N2 being the predominant subtype among isolates from LBMs. Phylogenetic analysis of the M-gene showed a high degree of nucleotide sequence identity with US isolates of AIVs but not with those of Asian or European lineages. While none of the isolates from wild birds had any antiviral resistance–associated mutations, 17 LBM isolates carried polymorphisms known to cause reduced susceptibility to antiviral drugs (adamantanes). Of these 17 isolates, 16 had S31N change and one isolate had V27A mutation.
Conclusions These results indicate independent evolution of M-gene in the absence of any antiviral drugs leading to mutations causing resistance indicating the need for continued active surveillance of AIVs.