Serological evidence of H9N2 avian influenza virus exposure among poultry workers from Fars province of Iran.

A Heidari,M Mancin,H Nili,G H Pourghanbari,S Leardini,I Monne,G Cattoli,K B Lankarani,A Piccirillo

doi:10.1186/s12985-016-0472-z

Abstract

BackgroundSince the 1990s, influenza A viruses of the H9N2 subtype have been causing infections in the poultry population around the globe. This influenza subtype is widely circulating in poultry and human cases of AI H9N2 have been sporadically reported in countries where this virus is endemic in domestic birds. The wide circulation of H9N2 viruses throughout Europe and Asia along with their ability to cause direct infection in mammals and humans, raises public health concerns. H9N2 AI was reported for the first time in Iran in 1998 and at present it is endemic in poultry. This study was carried out to evaluate the exposure to H9N2 AI viruses among poultry workers from the Fars province.Methods100 poultry workers and 100 healthy individuals with no professional exposure to poultry took part in this study. Serum samples were tested for antibodies against two distinct H9N2 avian influenza viruses, which showed different phylogenetic clustering and important molecular differences, such as at the amino acid (aa) position 226 (Q/L) (H3 numbering), using haemagglutination inhibition (HI) and microneutralization (MN) assays.ResultsResults showed that 17 % of the poultry workers were positive for the A/chicken/Iran/10VIR/854-5/2008 virus in MN test and 12 % in HI test using the titer ≥40 as positive cut-off value. Only 2 % of the poultry workers were positive for the A/chicken/Iran/12VIR/9630/1998 virus. Seroprevalence of non exposed individuals for both H9N2 strains was below 3 % by both tests. Statistical analyses models showed that exposure to poultry significantly increases the risk of infection with H9N2 virus.ConclusionsThe results have demonstrated that exposure to avian H9N2 viruses had occurred among poultry workers in the Fars province of Iran. Continuous surveillance programmes should be implemented to monitor the presence of avian influenza infections in humans and to evaluate their potential threat to poultry workers and public health.Electronic supplementary materialThe online version of this article (doi:10.1186/s12985-016-0472-z) contains supplementary material, which is available to authorized users.

Highlights

Since the 1990s, influenza A viruses of the H9N2 subtype have been causing infections in the poultry population around the globe
A significant proportion of recent H9N2 avian influenza (AI) isolates contains the L226Q (H3 numbering) amino acid substitution in their hemagglutinins (HAs) showing preferential binding to analogs of receptors with sialic acid linked to galactose by α2,6 linkage (SAα2,6Gal), a phenotypic portrait which is characteristic of human influenza viruses
The HA gene phylogenetic analysis of 88 Iranian H9N2 strains collected between 1998-2014 shows that they belong to two different groups of G1 lineage, named sublineage A and sub-lineage B for the purpose of this study (Fig. 1)

Summary

Introduction

Since the 1990s, influenza A viruses of the H9N2 subtype have been causing infections in the poultry population around the globe. The influenza A viruses of the H9N2 subtype are classified as low pathogenic avian influenza (LPAI) viruses They cause infections both in wild birds and in the poultry population worldwide, including several countries in Asia, Europe, North Africa and North America [6, 7]. A significant proportion of recent H9N2 avian influenza (AI) isolates contains the L226Q (H3 numbering) amino acid substitution in their hemagglutinins (HAs) showing preferential binding to analogs of receptors with sialic acid linked to galactose by α2,6 linkage (SAα2,6Gal), a phenotypic portrait which is characteristic of human influenza viruses These AI viruses might possess one of the key elements for infection in humans [8,9,10]. It has been reported that serial passages of an H9N2 virus through guinea pigs can result in the introduction of amino acid substitutions, which increases contact transmission efficiency in this mammalian model [21, 22]

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