Novel Avian Influenza H7N3 Strain Outbreak, British Columbia

Hirst, Martin; Astell, Caroline R.; Griffith, Malachi; Coughlin, Shaun; Moksa, Michelle; Zeng, Thomas; Smailus, Duane E.; Holt, Robert A.; Jones, Steven J.M.; Marra, Marco A.; Petric, Martin; Krajden, Mel; Lawrence, David; Mak, Annie; Chow, Ron; Skowronski, Danuta M.; Tweed, Sam; Goh, Swee-Han; Brunham, Robert C.; Robinson, John P.; Bowes, Victoria; Sojonky, Ken; Byrne, Seán; Li, Yanyan; Kobasa, Darwyn; Booth, Tim F.; Paetzel, Mark

doi:10.3201/eid1012.040743

Cited by 181 publications

(126 citation statements)

References 24 publications

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“…However, in this British Columbian outbreak, the recombination occurred between the HA and M genes (14). Two human cases of H7N3 infections have been reported.…”

Section: H7 Subtype: Shifts In Virulence Cause Health Concerns For Pomentioning

confidence: 99%

Microbial adaptation and change: avian influenza

Dj²

2004

Rev. Sci. Tech. OIE

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SummaryThe evolution of influenza is a continuing process involving viral and host factors. The increasing frequency of emergence of the highly pathogenic H5N1, H7N3 and H7N7 influenza viruses and the panzootic spread of H9N2 influenza virus, all of which can be potentially transmitted to humans, are of great concern to both veterinary and human public health officials. The question is how soon the next pandemic will emerge. A convergence of factors, including the population densities of poultry, pigs and humans, are likely factors affecting the evolution of the virus. Highly concentrated poultry and pig farming, in conjunction with traditional live animal or 'wet' markets, provide optimal conditions for increased mutation, reassortment and recombination of influenza viruses. Strategies to reduce the evolution of influenza and the emergence of pandemics include the separation of species, increased biosecurity, the development of new vaccine strategies and better basic knowledge of the virus. More effective co-operation between scientists and veterinary and public health officials is required to achieve these goals.

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“…However, in this British Columbian outbreak, the recombination occurred between the HA and M genes (14). Two human cases of H7N3 infections have been reported.…”

Section: H7 Subtype: Shifts In Virulence Cause Health Concerns For Pomentioning

confidence: 99%

Microbial adaptation and change: avian influenza

Dj²

2004

Rev. Sci. Tech. OIE

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“…Group 2 influenza A viruses include the H3 subtype, which further contains the seasonal H3N2 human strains, and the H7 subtype, which contains highly pathogenic avian influenza A viruses (4). Previously, infections with H7 viruses, through exposure to poultry, generally resulted in uncomplicated influenza illness and/or mild conjunctivitis (demonstrated for H7N3), with only one fatal case observed during an outbreak in The Netherlands (H7N7) (5,6). However in 2013, a novel influenza A virus (H7N9), the product of genetic reassortment of various avian strains, emerged in China.…”

Section: Introductionmentioning

confidence: 99%

Preexisting human antibodies neutralize recently emerged H7N9 influenza strains

Dunand¹,

Leon²,

Kaur³

et al. 2015

J. Clin. Invest.

118

138

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“…Cases of human infection by H7 influenza viruses have been reported sporadically since 1979 (51), caused by both low-and high-pathogenicity avian influenza (LPAI and HPAI, respectively) H7 viruses of the Eurasian and North American lineages. Outbreaks associated with human infections were reported in 2002 and 2003 in the United States (7,8), 2004 in Canada (7,23,49), in 1995 and 2006-2007 in the United Kingdom (1,15,27,33), in 2002 in Italy (37), and in 2003 in the Netherlands (17,25). The 2003 outbreak in the Netherlands was caused by an HPAI H7N7 subtype and was the source of infection for 89 people exposed to affected poultry, including three cases of possible human-to-human virus transmission (17).…”

mentioning

confidence: 99%

Structure and Receptor Complexes of the Hemagglutinin from a Highly Pathogenic H7N7 Influenza Virus

Yang

Carney

Donis

et al. 2012

J Virol

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Recurrence of highly pathogenic avian influenza (HPAI) virus subtype H7 in poultry continues to be a public health concern. In 2003, an HPAI H7N7 outbreak in the Netherlands infected 89 people in close contact with affected poultry and resulted in one fatal case. In previous studies, the virus isolated from this fatal case, A/Netherlands/219/2003 (NL219) caused a lethal infection in mouse models and had increased replication efficiency and a broader tissue distribution than nonlethal isolates from the same outbreak. A mutation which introduces a potential glycosylation site at Asn123 in the NL219 hemagglutinin was postulated to contribute to the pathogenic properties of this virus. To study this further, we have expressed the NL219 hemagglutinin in a baculovirus expression system and performed a structural analysis of the hemagglutinin in complex with avian and human receptor analogs. Glycan microarray and kinetic analysis were performed to compare the receptor binding profile of the wild-type recombinant NL219 HA to a variant with a threonine-to-alanine mutation at position 125, resulting in loss of the glycosylation site at Asn123. The results suggest that the additional glycosylation sequon increases binding affinity to avian-type ␣2-3-linked sialosides rather than switching to a human-like receptor specificity and highlight the mechanistic diversity of these pathogens, which calls attention to the need for further studies to fully understand the unique properties of these viruses.

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Novel Avian Influenza H7N3 Strain Outbreak, British Columbia

Cited by 181 publications

References 24 publications

Microbial adaptation and change: avian influenza

Microbial adaptation and change: avian influenza

Preexisting human antibodies neutralize recently emerged H7N9 influenza strains

Structure and Receptor Complexes of the Hemagglutinin from a Highly Pathogenic H7N7 Influenza Virus

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