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Original Articles

Genesis of avian influenza H9N2 in Bangladesh

, , , , , , , , & show all
Pages 1-17 | Received 23 Sep 2015, Accepted 02 Nov 2015, Published online: 25 Jan 2019
 

Abstract

Avian influenza subtype H9N2 is endemic in many bird species in Asia and the Middle East and has contributed to the genesis of H5N1, H7N9 and H10N8, which are potential pandemic threats. H9N2 viruses that have spread to Bangladesh have acquired multiple gene segments from highly pathogenic (HP) H7N3 viruses that are presumably in Pakistan and currently cocirculate with HP H5N1. However, the source and geographic origin of these H9N2 viruses are not clear. We characterized the complete genetic sequences of 37 Bangladeshi H9N2 viruses isolated in 2011–2013 and investigated their inter- and intrasubtypic genetic diversities by tracing their genesis in relationship to other H9N2 viruses isolated from neighboring countries. H9N2 viruses in Bangladesh are homogenous with several mammalian host-specific markers and are a new H9N2 sublineage wherein the hemagglutinin (HA) gene is derived from an Iranian H9N2 lineage (Mideast_B Iran), the neuraminidase (NA) and polymerase basic 2 (PB2) genes are from Dubai H9N2 (Mideast_C Dubai), and the non-structural protein (NS), nucleoprotein (NP), matrix protein (MP), polymerase acidic (PA) and polymerase basic 1 (PB1) genes are from HP H7N3 originating from Pakistan. Different H9N2 genotypes that were replaced in 2006 and 2009 by other reassortants have been detected in Bangladesh. Phylogenetic and molecular analyses suggest that the current genotype descended from the prototypical H9N2 lineage (G1), which circulated in poultry in China during the late 1990s and came to Bangladesh via the poultry trade within the Middle East, and that this genotype subsequently reassorted with H7N3 and H9N2 lineages from Pakistan and spread throughout India. Thus, continual surveillance of Bangladeshi HP H5N1, H7N3 and H9N2 is warranted to identify further evolution and adaptation to humans.

We thank Jerry Parker, Richard Elia and Mark Weilnau for maintaining the influenza database at St Jude Children’s Research Hospital, Memphis, USA; James Knowles for administrative assistance; and Vani Shanker for scientific editing. This work was supported by Contract NO HHSN266200700005C from the National Institute of Allergy and Infectious Disease, National Institutes of Health, Department of Health and Human Services, and by the American Lebanese Syrian Associated Charities. The nucleotide sequences obtained in this study have been deposited in GenBank and are available for download using accession numbers KJ643594–KJ643868.

Supplementary Information for this article can be found on Emerging Microbes & Infections's website (http://www.nature.com/emi/).