Dataset Information

Changes in adaptation of H5N2 highly pathogenic avian influenza H5 clade 2.3.4.4 viruses in chickens and mallards.

ABSTRACT: H5N2 highly pathogenic avian influenza (HPAI) viruses caused a severe poultry outbreak in the United States (U.S.) during 2015. In order to examine changes in adaptation of this viral lineage, the infectivity, pathogenicity and transmission of poultry H5N2 viruses were investigated in chickens and mallards in comparison to the wild duck 2014 U.S. index H5N2 virus. The four poultry isolates examined had a lower mean bird infectious dose than the index virus but still transmitted poorly to direct contacts. In mallards, two of the H5N2 poultry isolates had similar high infectivity and transmissibility as the index H5N2 virus, the H5N8 U.S. index virus, and a 2005 H5N1 clade 2.2 virus. Mortality occurred with the H5N1 virus and, interestingly, with one of two poultry H5N2 isolates. Increased virus adaptation to chickens was observed with the poultry H5N2 viruses; however these viruses retained high adaptation to mallards but pathogenicity was differently affected.

SUBMITTER: DeJesus E

PROVIDER: S-EPMC5102764 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Changes in adaptation of H5N2 highly pathogenic avian influenza H5 clade 2.3.4.4 viruses in chickens and mallards.

DeJesus Eric E Costa-Hurtado Mar M Smith Diane D Lee Dong-Hun DH Spackman Erica E Kapczynski Darrell R DR Torchetti Mia Kim MK Killian Mary L ML Suarez David L DL Swayne David E DE Pantin-Jackwood Mary J MJ

Virology 20160912

H5N2 highly pathogenic avian influenza (HPAI) viruses caused a severe poultry outbreak in the United States (U.S.) during 2015. In order to examine changes in adaptation of this viral lineage, the infectivity, pathogenicity and transmission of poultry H5N2 viruses were investigated in chickens and mallards in comparison to the wild duck 2014 U.S. index H5N2 virus. The four poultry isolates examined had a lower mean bird infectious dose than the index virus but still transmitted poorly to direct ...[more]

PMID: 27632565

Similar Datasets

Project description:The H5N8 highly pathogenic avian influenza (HPAI) clade 2.3.4.4 virus spread to North America by wild birds and reassorted to generate the H5N2 HPAI virus that caused the poultry outbreak in the United States in 2015. In previous studies, we showed that H5N2 viruses isolated from poultry in the later stages of the outbreak had higher infectivity and transmissibility in chickens than the wild bird index H5N2 virus. Here, we determined the genetic changes that contributed to the difference in host virus fitness by analyzing sequence data from all of the viruses detected during the H5N2 outbreak, and studying the pathogenicity of reassortant viruses generated with the index wild bird virus and a chicken virus from later in the outbreak. Viruses with the wild bird virus backbone and either PB1, NP, or the entire polymerase complex of the chicken isolate, caused higher and earlier mortality in chickens, with three mutations (PB1 E180D, M317V, and NP I109T) identified to increase polymerase activity in chicken cells. The reassortant virus with the HA and NA from the chicken virus, where mutations in functionally known gene regions were acquired as the virus circulated in turkeys (HA S141P and NA S416G) and later in chickens (HA M66I, L322Q), showed faster virus growth, bigger plaque size and enhanced heat persistence in vitro, and increased pathogenicity and transmissibility in chickens. Collectively, these findings demonstrate an evolutionary pathway in which a HPAI virus from wild birds can accumulate genetic changes to increase fitness in poultry.IMPORTANCE H5Nx highly pathogenic avian influenza (HPAI) viruses of the A/goose/Guangdong/1/96 lineage continue to circulate widely affecting both poultry and wild birds. These viruses continue to change and reassort, which affects their fitness to different avian hosts. In this study, we defined mutations associated with increased virus fitness in chickens as the clade 2.3.4.4. H5N2 HPAI virus circulated in different avian species. We identified mutations in the PB1, NP, HA, and NA virus proteins that were highly conserved in the poultry isolates and contributed to the adaptation of this virus in chickens. This knowledge is important for understanding the epidemiology of H5Nx HPAI viruses and specifically the changes related to adaptation of these viruses in poultry.

Project description:Wild aquatic birds have been associated with the intercontinental spread of H5 subtype highly pathogenic avian influenza (HPAI) viruses of the A/goose/Guangdong/1/96 (Gs/GD) lineage during 2005, 2010, and 2014, but dispersion by wild waterfowl has not been implicated with spread of other HPAI viruses. To better understand why Gs/GD H5 HPAI viruses infect and transmit more efficiently in waterfowl than other HPAI viruses, groups of mallard ducks were challenged with one of 14 different H5 and H7 HPAI viruses, including a Gs/GD lineage H5N1 (clade 2.2) virus from Mongolia, part of the 2005 dispersion, and the H5N8 and H5N2 index HPAI viruses (clade 2.3.4.4) from the United States, part of the 2014 dispersion. All virus-inoculated ducks and contact exposed ducks became infected and shed moderate to high titers of the viruses, with the exception that mallards were resistant to Ck/Pennsylvania/83 and Ck/Queretaro/95 H5N2 HPAI virus infection. Clinical signs were only observed in ducks challenged with the H5N1 2005 virus, which all died, and with the H5N8 and H5N2 2014 viruses, which had decreased weight gain and fever. These three viruses were also shed in higher titers by the ducks, which could facilitate virus transmission and spread. This study highlights the possible role of wild waterfowl in the spread of HPAI viruses. IMPORTANCE:The spread of H5 subtype highly pathogenic avian influenza (HPAI) viruses of the Gs/GD lineage by migratory waterfowl is a serious concern for animal and public health. H5 and H7 HPAI viruses are considered to be adapted to gallinaceous species (chickens, turkeys, quail, etc.) and less likely to infect and transmit in wild ducks. In order to understand why this is different with certain Gs/GD lineage H5 HPAI viruses, we compared the pathogenicity and transmission of several H5 and H7 HPAI viruses from previous poultry outbreaks to Gs/GD lineage H5 viruses, including H5N1 (clade 2.2), H5N8 and H5N2 (clade 2.3.4.4) viruses, in mallards as a representative wild duck species. Surprisingly, most HPAI viruses examined in this study replicated well and transmitted among mallards; however, the three Gs/GD lineage H5 HPAI viruses replicated to higher titers, which could explain the transmission of these viruses in susceptible wild duck populations.

Project description:Highly pathogenic avian influenza (HPAI) viruses from the H5Nx Goose/Guangdong/96 lineage continue to cause outbreaks in domestic and wild bird populations. Two distinct genetic groups of H5N8 HPAI viruses, hemagglutinin (HA) clades 2.3.4.4A and 2.3.4.4B, caused intercontinental outbreaks in 2014 to 2015 and 2016 to 2017, respectively. Experimental infections using viruses from these outbreaks demonstrated a marked difference in virulence in mallards, with the H5N8 virus from 2014 causing mild clinical disease and the 2016 H5N8 virus causing high mortality. To assess which gene segments are associated with enhanced virulence of H5N8 HPAI viruses in mallards, we generated reassortant viruses with 2014 and 2016 viruses. For single-segment reassortants in the genetic backbone of the 2016 virus, pathogenesis experiments in mallards revealed that morbidity and mortality were reduced for all eight single-segment reassortants compared to the parental 2016 virus, with significant reductions in mortality observed with the polymerase basic protein 2 (PB2), nucleoprotein (NP), and matrix (M) reassortants. No differences in morbidity and mortality were observed with reassortants that either have the polymerase complex segments or the HA and neuraminidase (NA) segments of the 2016 virus in the genetic backbone of the 2014 virus. In vitro assays showed that the NP and polymerase acidic (PA) segments of the 2014 virus lowered polymerase activity when combined with the polymerase complex segments of the 2016 virus. Furthermore, the M segment of the 2016 H5N8 virus was linked to filamentous virion morphology. Phylogenetic analyses demonstrated that gene segments related to the more virulent 2016 H5N8 virus have persisted in the contemporary H5Nx HPAI gene pool until 2020. IMPORTANCE Outbreaks of H5Nx HPAI viruses from the goose/Guangdong/96 lineage continue to occur in many countries and have resulted in substantial impact on wild birds and poultry. Epidemiological evidence has shown that wild waterfowl play a major role in the spread of these viruses. While HPAI virus infection in gallinaceous species causes high mortality, a wide range of disease outcomes has been observed in waterfowl species. In this study, we examined which gene segments contribute to severe disease in mallards infected with H5N8 HPAI viruses. No virus gene was solely responsible for attenuating the high virulence of a 2016 H5N8 virus, but the PB2, NP, and M segments significantly reduced mortality. The findings herein advance our knowledge on the pathobiology of avian influenza viruses in waterfowl and have potential implications on the ecology and epidemiology of H5Nx HPAI in wild bird populations.

Dataset Information

Changes in adaptation of H5N2 highly pathogenic avian influenza H5 clade 2.3.4.4 viruses in chickens and mallards.

Publications

Changes in adaptation of H5N2 highly pathogenic avian influenza H5 clade 2.3.4.4 viruses in chickens and mallards.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets