Genetic and Antigenic Characteristics of Highly Pathogenic Avian Influenza A(H5N8) Viruses Circulating in Domestic Poultry in Egypt, 2017-2021.

Ahmed Kandeil,Mohamed El Sayes,Ghazi Kayali,Mohamed A Ali,Rabeh El-Shesheny,Richard J Webby,Ahmed El Taweel,Yassmin Moatasim,Pamela P Mckenzie,Adam Rubrum,Trushar Jeevan

doi:10.3390/microorganisms10030595

Ahmed Kandeil, Mohamed El Sayes + Show 9 more

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https://doi.org/10.3390/microorganisms10030595

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Abstract

In Egypt, the endemicity of avian influenza viruses is a serious concern. Since 2016, several outbreaks of H5N8 have been recorded among domestic poultry in various areas of the country. Active surveillance of domestic poultry across several governorates in Egypt from 2017 to 2021 detected at least six genotypes of Highly Pathogenic Avian Influenza (HPAI) H5N8 viruses with evidence of partial or complete annual replacement of dominant strains. Although all Egyptian H5N8 viruses had clade 2.3.4.4b hemagglutinin (HA) genes, the remaining viral gene segments were from multiple geographic origins, indicating that the H5N8 isolates resulted from multiple introductions. Mutations in the viral proteins associated with pathogenicity and antiviral drug resistance were detected. Some mutations in the HA resulted in antigenic drift. Heterogeneity in circulating H5N8 HPAI threatens poultry production and public health.

Highlights

Pathogenic Avian Influenza (HPAI) H5 viruses were first detected in chickens in Scotland in 1959 and sporadically thereafter, with limited spread at each instance [1]. in 1996, the Highly Pathogenic Avian Influenza (HPAI) A/goose/Guangdong/1/96 (H5N1) virus was detected
We identify the genetic and antigenic characteristics of HPAI H5N8 viruses collected during active surveillance activities in Egypt between 2017 and 2021
No reassortment event was characterized through our extensive analysis of 96 Egyptian HPAI H5N8 viruses of the current study and endemic AI H5N1 and H9N2 viruses in

Summary

Introduction

Pathogenic Avian Influenza (HPAI) H5 viruses were first detected in chickens in Scotland in 1959 and sporadically thereafter, with limited spread at each instance [1]. In 1996, the HPAI A/goose/Guangdong/1/96 (H5N1) virus was detected. It caused death in infected domestic and wild birds and acquired the ability to cross the species barrier and infect humans [2,3]. Descendants of these viruses spread globally, continued circulating, and have evolved into multiple genetically distinct clades (0–9) and subclades. The HPAI viruses bearing an HA of clade 2.3.4.4 have acquired several types of neuraminidases (NAs) including N1, N2, N5, N6, and N8 by reassortment events with other Low Pathogenic

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