Phylogenetic and molecular analysis of highly pathogenic avian influenza H5N8 and H5N5 viruses detected in Poland in 2016-2017

Świętoń, Edyta; Śmietanka, Krzysztof

doi:10.1111/tbed.12924

Cited by 22 publications

(26 citation statements)

References 25 publications

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“…The first actual detections of BABAB8AA were in Croatia, Hungary, and France from October 2016. This virus was later detected farther north, in Germany and Poland in winter 2016 to 2017 ( 20 , 33 ). This suggests that the reassortant spread in a restricted part of Europe during late autumn migration and the wintering period and potentially involved spillback of gene segments from domestic anseriforms to wild birds, possibly in Hungary.…”

Section: Resultsmentioning

confidence: 99%

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Genesis and spread of multiple reassortants during the 2016/2017 H5 avian influenza epidemic in Eurasia

Lycett

Pohlmann

Staubach

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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Highly pathogenic avian influenza (HPAI) viruses of the H5 A/goose/Guangdong/1/96 lineage can cause severe disease in poultry and wild birds, and occasionally in humans. In recent years, H5 HPAI viruses of this lineage infecting poultry in Asia have spilled over into wild birds and spread via bird migration to countries in Europe, Africa, and North America. In 2016/2017, this spillover resulted in the largest HPAI epidemic on record in Europe and was associated with an unusually high frequency of reassortments between H5 HPAI viruses and cocirculating low-pathogenic avian influenza viruses. Here, we show that the seven main H5 reassortant viruses had various combinations of gene segments 1, 2, 3, 5, and 6. Using detailed time-resolved phylogenetic analysis, most of these gene segments likely originated from wild birds and at dates and locations that corresponded to their hosts’ migratory cycles. However, some gene segments in two reassortant viruses likely originated from domestic anseriforms, either in spring 2016 in east China or in autumn 2016 in central Europe. Our results demonstrate that, in addition to domestic anseriforms in Asia, both migratory wild birds and domestic anseriforms in Europe are relevant sources of gene segments for recent reassortant H5 HPAI viruses. The ease with which these H5 HPAI viruses reassort, in combination with repeated spillovers of H5 HPAI viruses into wild birds, increases the risk of emergence of a reassortant virus that persists in wild bird populations yet remains highly pathogenic for poultry.

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Section: Resultsmentioning

confidence: 99%

“…Throughout Europe, this virus caused both massive die-offs in wild birds and outbreaks in poultry farms, lasting until at least summer 2017 ( 8 , 20 , 27 – 33 ).…”

Section: Resultsmentioning

confidence: 99%

Genesis and spread of multiple reassortants during the 2016/2017 H5 avian influenza epidemic in Eurasia

Lycett

Pohlmann

Staubach

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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“…This could have partially contributed to the limited number of H5N8 HPAIV outbreaks in chicken holdings during the 2016-2017 epidemics in Europe (12% of the total reported outbreaks), in comparison with its detections in waterfowl holdings, including in Spain [5]. However, different genotypes of H5N8 HPAIV circulated in Europe at that time [30]. Therefore, important differences in the biological properties and virulence of H5N8 HPAIV between European strains may exist.…”

Section: Discussionmentioning

confidence: 99%

Pathobiology of the highly pathogenic avian influenza viruses H7N1 and H5N8 in different chicken breeds and role of Mx 2032 G/A polymorphism in infection outcome

Sánchez-González

Ramis

Nofrarías

et al. 2020

Vet Res

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Chickens are highly susceptible to highly pathogenic avian influenza viruses (HPAIVs). However, the severity of infection varies depending of the viral strain and the genetic background of the host. In this study, we evaluated the pathogenesis of two HPAIVs (H7N1 and H5N8) and assessed the susceptibility to the infection of local and commercial chicken breeds from Spain. Eight chicken breeds were intranasally inoculated with 105 ELD50 of A/Chicken/Italy/5093/1999 (H7N1) or A/Goose/Spain/IA17CR02699/2017 (H5N8 clade 2.3.4.4. B) and monitored during 10 days. Chickens were highly susceptible to both HPAIVs, but H7N1 was considerably more virulent than H5N8 as demonstrated by the highest mortality rates and shortest mean death times (MDT). Both HPAIVs produced severe necrosis and intense viral replication in the central nervous system, heart and pancreas; however, the lesions and replication in other tissues were virus-dependent. High levels of viral RNA were detected by the oral route with both viruses. In contrast, a low number of H5N8-inoculated chickens shed by the cloacal route, demonstrating a different pattern of viral shedding dependent of the HPAIV. We found a high variation in the susceptibility to HPAIVs between the different chicken breeds. The birds carrying the genotype AA and AG at position 2032 in chicken Mx gene presented a slightly higher, but not significant, percentage of survival and a statistically significant longer MDT than GG individuals. Our study demonstrated that the severity of HPAI infection is largely dependent of the viral isolate and host factors, underlining the complexity of HPAI infections.

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“…During the HPAI H5N8 clade 2.3.4.4 group B epizootic in 2016–2017, multiple reassortant variants of subtype H5N5 were detected in Europe [19,20,21,22,23,24,25,26]. However, the number of birds detected with HPAI H5N5 virus was limited compared to H5N8 [19].…”

Section: Introductionmentioning

confidence: 99%

Spread of Highly Pathogenic Avian Influenza (HPAI) H5N5 Viruses in Europe in 2016–2017 Appears Related to the Timing of Reassortment Events

Bergervoet

Heutink

et al. 2019

Viruses

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During the epizootic of highly pathogenic avian influenza (HPAI) H5N8 virus in Europe in 2016–2017, HPAI viruses of subtype H5N5 were also isolated. However, the detection of H5N5 viruses was limited compared to H5N8. In this study, we show that the genetic constellation of a newly isolated H5N5 virus is different from two genotypes previously identified in the Netherlands. The introduction and spread of the three H5N5 genotypes in Europe was studied using spatiotemporal and genetic analysis. This demonstrated that the genotypes were isolated in distinguishable phases of the epizootic, and suggested multiple introductions of H5N5 viruses into Europe followed by local spread. We estimated the timing of the reassortment events, which suggested that the genotypes emerged after the start of autumn migration. This may have prevented large-scale spread of the H5N5 viruses on wild bird breeding sites before introduction into Europe. Experiments in primary chicken and duck cells revealed only minor differences in cytopathogenicity and replication kinetics between H5N5 genotypes and H5N8. These results suggest that the limited spread of HPAI H5N5 viruses is related to the timing of the reassortment events rather than changes in virus pathogenicity or replication kinetics.

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Phylogenetic and molecular analysis of highly pathogenic avian influenza H5N8 and H5N5 viruses detected in Poland in 2016-2017

Cited by 22 publications

References 25 publications

Genesis and spread of multiple reassortants during the 2016/2017 H5 avian influenza epidemic in Eurasia

Genesis and spread of multiple reassortants during the 2016/2017 H5 avian influenza epidemic in Eurasia

Pathobiology of the highly pathogenic avian influenza viruses H7N1 and H5N8 in different chicken breeds and role of Mx 2032 G/A polymorphism in infection outcome

Spread of Highly Pathogenic Avian Influenza (HPAI) H5N5 Viruses in Europe in 2016–2017 Appears Related to the Timing of Reassortment Events

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