scholarly journals Emergence and Selection of a Highly Pathogenic Avian Influenza H7N3 Virus

Proceedings ◽  
2020 ◽  
Vol 50 (1) ◽  
pp. 46
Author(s):  
Nancy Beerens ◽  
Rene Heutink ◽  
Ben Peeters
Keyword(s):  
Avian Influenza ◽  
Clinical Symptoms ◽  
Virus Preparation ◽  
Full Genome Sequencing ◽  
Highly Pathogenic ◽  
Pathogenic Avian Influenza ◽  
Pathogenic Virus ◽  
Nucleotide Insertion ◽  
H7n3 Virus ◽  
Selection Of

Low pathogenic avian influenza (LPAI) viruses of subtypes H5 and H7 have the ability to spontaneously mutate into highly pathogenic (HPAI) variants, causing high mortality in poultry. The switch to high pathogenicity is poorly understood, and evidence from the field is scarce. This study provides direct evidence for LPAI to HPAI mutation from a turkey farm during an H7N3 outbreak in the Netherlands. At the farm, only mild clinical symptoms were reported, but the intravenous pathogenicity index measured for the virus isolated from the infected turkeys was consistent with a highly pathogenic virus. Using deep-sequencing, we showed that a minority of HPAI virus (0.06%) was present in the virus preparation. Analysis of different organs of the infected turkeys showed the highest percentage of HPAI virus was present in the lung (4.4%). The HPAI virus contained a 12-nucleotide insertion in the hemagglutinin (HA) cleavage site that was introduced by a single event, as no intermediates with shorter inserts were identified. The HPAI virus was rapidly selected in chickens, after both intravenous and intranasal/intratracheal inoculation with the mixed virus preparation. Full-genome sequencing revealed that both pathotypes contained a deletion in the stalk region of the neuraminidase protein. We identified mutations in HA and polymerase basic protein 1 (PB1) in the HPAI virus, which were already present as minority variants in the LPAI virus. Our findings provide more insight into the molecular changes and mechanisms involved in the emergence of HPAI viruses. This knowledge may be used for the timely identification of LPAI viruses that pose a risk of becoming highly pathogenic in the field.

scholarly journals Emergence and Selection of a Highly Pathogenic Avian Influenza H7N3 Virus

2020 ◽  
Vol 94 (8) ◽  
Author(s):  
Nancy Beerens ◽  
Rene Heutink ◽  
Frank Harders ◽  
Alex Bossers ◽  
Guus Koch ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Cleavage Site ◽  
Highly Pathogenic Avian Influenza ◽  
Severe Disease ◽  
Virus Population ◽  
Highly Pathogenic ◽  
Pathogenic Avian Influenza ◽  
High Pathogenicity ◽  
H7n3 Virus ◽  
Selection Of

ABSTRACT Low-pathogenicity avian influenza (LPAI) viruses of subtypes H5 and H7 have the ability to spontaneously mutate to highly pathogenic (HPAI) virus variants, causing high mortality in poultry. The highly pathogenic phenotype is caused by mutation of the hemagglutinin (HA) cleavage site, but additional mutations may play a role. Evidence from the field for the switch to high pathogenicity remains scarce. This study provides direct evidence for LPAI-to-HPAI virus mutation during H7N3 infection of a turkey farm in the Netherlands. No severe clinical symptoms were reported at the farm, but deep sequencing of isolates from the infected turkeys revealed a minority of HPAI virus sequences (0.06%) in the virus population. The HPAI virus contained a 12-nucleotide insertion in the HA cleavage site that was likely introduced by a single event as no intermediates with shorter inserts were identified. This suggests nonhomologous recombination as the mechanism of insertion. Analysis of different organs of the infected turkeys showed the largest amount of HPAI virus in the lung (4.4%). The HPAI virus was rapidly selected in experimentally infected chickens after both intravenous and intranasal/intratracheal inoculation with a mixed virus preparation. Full-genome sequencing revealed that both pathotypes contained a deletion in the stalk region of the neuraminidase protein. We identified additional mutations in HA and polymerase basic protein 1 (PB1) in the HPAI virus, which were already present as minority variants in the LPAI virus population. Our findings provide more insight into the molecular changes and mechanisms involved in the emergence and selection of HPAI viruses. IMPORTANCE Low-pathogenicity avian influenza (LPAI) viruses circulate in wild birds and can be transmitted to poultry. LPAI viruses can mutate to become highly pathogenic avian influenza (HPAI) viruses causing severe disease and death in poultry. Little is known about this switch to high pathogenicity. We isolated an LPAI H7N3 virus from an infected turkey farm and showed that this contains small amounts of HPAI virus. The HPAI virus rapidly outcompeted the LPAI virus in chickens that were experimentally infected with this mixture of viruses. We analyzed the genome sequences of the LPAI and HPAI viruses and identified several changes that may be important for a virus to become highly pathogenic. This knowledge may be used for timely identification of LPAI viruses that pose a risk of becoming highly pathogenic in the field.

scholarly journals Highly Pathogenic Avian Influenza A(H7N3) Virus in Poultry Workers, Mexico, 2012

2013 ◽  
Vol 19 (9) ◽  
Author(s):  
Irma Lopez-Martinez ◽  
Amanda Balish ◽  
Gisela Barrera-Badillo ◽  
Joyce Jones ◽  
Tatiana E. Nuñez-García ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Influenza A ◽  
Highly Pathogenic Avian Influenza ◽  
Highly Pathogenic ◽  
Pathogenic Avian Influenza ◽  
Poultry Workers ◽  
H7n3 Virus

scholarly journals Loss of Fitness of Mexican H7N3 Highly Pathogenic Avian Influenza Virus in Mallards after Circulating in Chickens

2019 ◽  
Vol 93 (14) ◽  
Author(s):  
Sung-Su Youk ◽  
Dong-Hun Lee ◽  
Christina M. Leyson ◽  
Diane Smith ◽  
Miria Ferreira Criado ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Highly Pathogenic Avian Influenza ◽  
Clinical Signs ◽  
Host Adaptation ◽  
Avian Species ◽  
Full Genome Sequencing ◽  
Highly Pathogenic ◽  
Pathogenic Avian Influenza ◽  
Large Populations

ABSTRACTOutbreaks of highly pathogenic avian influenza (HPAI) virus subtype H7N3 have been occurring in commercial chickens in Mexico since its first introduction in 2012. In order to determine changes in virus pathogenicity and adaptation in avian species, three H7N3 HPAI viruses from 2012, 2015, and 2016 were evaluated in chickens and mallards. All three viruses caused high mortality in chickens when given at medium to high doses and replicated similarly. No mortality or clinical signs and similar infectivity were observed in mallards inoculated with the 2012 and 2016 viruses. However, the 2012 H7N3 HPAI virus replicated well in mallards and transmitted to contacts, whereas the 2016 virus replicated poorly and did not transmit to contacts, which indicates that the 2016 virus is less adapted to mallards.In vitro, the 2016 virus grew slower and to lower titers than did the 2012 virus in duck fibroblast cells. Full-genome sequencing showed 115 amino acid differences between the 2012 and the 2016 viruses, with some of these changes previously associated with changes in replication in avian species, including hemagglutinin (HA) A125T, nucleoprotein (NP) M105V, and NP S377N. In conclusion, as the Mexican H7N3 HPAI virus has passaged through large populations of chickens in a span of several years and has retained its high pathogenicity for chickens, it has decreased in fitness in mallards, which could limit the potential spread of this HPAI virus by waterfowl.IMPORTANCENot much is known about changes in host adaptation of avian influenza (AI) viruses in birds after long-term circulation in chickens or other terrestrial poultry. Although the origin of AI viruses affecting poultry is wild aquatic birds, the role of these birds in further dispersal of poultry-adapted AI viruses is not clear. Previously, we showed that HPAI viruses isolated early from poultry outbreaks could still infect and transmit well in mallards. In this study, we demonstrate that the Mexican H7N3 HPAI virus after four years of circulation in chickens replicates poorly and does not transmit in mallards but remains highly pathogenic in chickens. This information on changes in host adaptation is important for understanding the epidemiology of AI viruses and the role that wild waterfowl may play in disseminating viruses adapted to terrestrial poultry.

scholarly journals Intersegmental recombination between the haemagglutinin and matrix genes was responsible for the emergence of a highly pathogenic H7N3 avian influenza virus in British Columbia

2005 ◽  
Vol 86 (3) ◽  
pp. 727-731 ◽  
Author(s):  
John Pasick ◽  
Katherine Handel ◽  
John Robinson ◽  
John Copps ◽  
Deidre Ridd ◽  
...  
Keyword(s):  
British Columbia ◽  
Influenza Virus ◽  
Homologous Recombination ◽  
Avian Influenza ◽  
Avian Influenza Virus ◽  
Highly Pathogenic Avian Influenza ◽  
Highly Pathogenic ◽  
Pathogenic Avian Influenza ◽  
Pathogenic Viruses ◽  
H7n3 Virus

In February 2004 a highly pathogenic avian influenza (HPAI) outbreak erupted in British Columbia. Investigations indicated that the responsible HPAI H7N3 virus emerged suddenly from a low pathogenic precursor. Analysis of the haemagglutinin (HA) genes of the low and high pathogenic viruses isolated from the index farm revealed the only difference to be a 21 nt insert at the HA cleavage site of the highly pathogenic avian influenza virus. It was deduced that this insert most probably arose as a result of non-homologous recombination between the HA and matrix genes of the same virus. Over the course of the outbreak, a total of 37 isolates with, and 3 isolates without inserts were characterized. The events described here appear very similar to those which occurred in Chile in 2002 where the virulence shift of another H7N3 virus was attributed to non-homologous recombination between the HA and nucleoprotein genes.

Sign in / Sign up

Export Citation Format

Share Document