scholarly journals Highly Pathogenic Avian Influenza A(H5N6) Virus Clade 2.3.4.4h in Wild Birds and Live Poultry Markets, Bangladesh

2021 ◽  
Vol 27 (9) ◽  
pp. 2492-2494
Author(s):  
Jasmine C.M. Turner ◽  
Subrata Barman ◽  
Mohammed M. Feeroz ◽  
M. Kamrul Hasan ◽  
Sharmin Akhtar ◽  
...  
2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Knut Madslien ◽  
Torfinn Moldal ◽  
Britt Gjerset ◽  
Sveinn Gudmundsson ◽  
Arne Follestad ◽  
...  

Abstract Background Several outbreaks of highly pathogenic avian influenza (HPAI) caused by influenza A virus of subtype H5N8 have been reported in wild birds and poultry in Europe during autumn 2020. Norway is one of the few countries in Europe that had not previously detected HPAI virus, despite widespread active monitoring of both domestic and wild birds since 2005. Results We report detection of HPAI virus subtype H5N8 in a wild pink-footed goose (Anser brachyrhynchus), and several other geese, ducks and a gull, from south-western Norway in November and December 2020. Despite previous reports of low pathogenic avian influenza (LPAI), this constitutes the first detections of HPAI in Norway. Conclusions The mode of introduction is unclear, but a northward migration of infected geese or gulls from Denmark or the Netherlands during the autumn of 2020 is currently our main hypothesis for the introduction of HPAI to Norway. The presence of HPAI in wild birds constitutes a new, and ongoing, threat to the Norwegian poultry industry, and compliance with the improved biosecurity measures on poultry farms should therefore be ensured. [MK1]Finally, although HPAI of subtype H5N8 has been reported to have very low zoonotic potential, this is a reminder that HPAI with greater zoonotic potential in wild birds may pose a threat in the future. [MK1]Updated with a sentence emphasizing the risk HPAI pose to poultry farms, both in the Abstract and in the Conclusion-section in main text, as suggested by Reviewer 1 (#7).


2015 ◽  
Vol 21 (5) ◽  
pp. 775-780 ◽  
Author(s):  
Hye-Ryoung Kim ◽  
Yong-Kuk Kwon ◽  
Il Jang ◽  
Youn-Jeong Lee ◽  
Hyun-Mi Kang ◽  
...  

2021 ◽  
Vol 27 (11) ◽  
pp. 2940-2943
Author(s):  
Guimei He ◽  
Le Ming ◽  
Xiang Li ◽  
Yuhe Song ◽  
Ling Tang ◽  
...  

2017 ◽  
Vol 23 (12) ◽  
pp. 2050-2054 ◽  
Author(s):  
Erik Kleyheeg ◽  
Roy Slaterus ◽  
Rogier Bodewes ◽  
Jolianne M. Rijks ◽  
Marcel A.H. Spierenburg ◽  
...  

2017 ◽  
Vol 98 (7) ◽  
pp. 1573-1586 ◽  
Author(s):  
Ahmed Kandeil ◽  
Ahmed Kayed ◽  
Yassmin Moatasim ◽  
Richard J. Webby ◽  
Pamela P. McKenzie ◽  
...  

2020 ◽  
Vol 94 (11) ◽  
Author(s):  
René M. Vigeveno ◽  
Marjolein J. Poen ◽  
Edyth Parker ◽  
Melle Holwerda ◽  
Karen de Haan ◽  
...  

ABSTRACT Highly pathogenic avian influenza A(H5N8) viruses first emerged in China in 2010 and in 2014 spread throughout Asia and to Europe and the United States via migrating birds. Influenza A(H5N8) viruses were first detected in the Netherlands in 2014 and caused five outbreaks in poultry farms but were infrequently detected in wild birds. In 2016, influenza A(H5N8) viruses were reintroduced into the Netherlands, resulting in eight poultry farm outbreaks. This outbreak resulted in numerous dead wild birds with severe pathology. Phylogenetic analysis showed that the polymerase genes of these viruses had undergone extensive reassortment between outbreaks. Here, we investigated the differences in virulence between the 2014-15 and the 2016-17 outbreaks by characterizing the polymerase complex of influenza A(H5N8) viruses from both outbreaks. We found that viruses from the 2014-15 outbreak had significantly higher polymerase complex activity in both human and avian cell lines than did those from the 2016-17 outbreak. No apparent differences in the balance between transcription and replication of the viral genome were observed. Interestingly, the 2014-15 polymerase complexes induced significantly higher levels of interferon beta (IFN-β) than the polymerase complexes of the 2016-17 outbreak viruses, mediated via retinoic acid-inducible gene I (RIG-I). Inoculation of primary duck cells with recombinant influenza A(H5N8) viruses, including viruses with reassorted polymerase complexes, showed that the polymerase complexes from the 2014-15 outbreak induced higher levels of IFN-β despite relatively minor differences in replication capacity. Together, these data suggest that despite the lower levels of polymerase activity, the higher 2016-17 influenza A(H5N8) virus virulence may be attributed to the lower level of activation of the innate immune system. IMPORTANCE Compared to the 2014-15 outbreak, the 2016-17 outbreak of influenza A(H5N8) viruses in the Netherlands and Europe was more virulent; the number of dead or diseased wild birds found and the severity of pathological changes were higher during the 2016-17 outbreak. The polymerase complex plays an important role in influenza virus virulence, and the gene segments of influenza A(H5N8) viruses reassorted extensively between the outbreaks. In this study, the 2014-15 polymerase complexes were found to be more active, which is counterintuitive with the observed higher virulence of the 2016-17 outbreak viruses. Interestingly, the 2014-15 polymerase complexes also induced higher levels of IFN-β. These findings suggest that the higher virulence of influenza A(H5N8) viruses from the 2016-17 outbreak may be related to the lower induction of IFN-β. An attenuated interferon response could lead to increased dissemination, pathology, and mortality, as observed in (wild) birds infected during the 2016-2017 outbreak.


2020 ◽  
Vol 94 (23) ◽  
Author(s):  
Rabeh El-Shesheny ◽  
John Franks ◽  
Jasmine Turner ◽  
Patrick Seiler ◽  
David Walker ◽  
...  

ABSTRACT The genesis of novel influenza viruses through reassortment poses a continuing risk to public health. This is of particular concern in Bangladesh, where highly pathogenic avian influenza viruses of the A(H5N1) subtype are endemic and cocirculate with other influenza viruses. Active surveillance of avian influenza viruses in Bangladeshi live poultry markets detected three A(H5) genotypes, designated H5N1-R1, H5N1-R2, and H5N2-R3, that arose from reassortment of A(H5N1) clade 2.3.2.1a viruses. The H5N1-R1 and H5N1-R2 viruses contained HA, NA, and M genes from the A(H5N1) clade 2.3.2.1a viruses and PB2, PB1, PA, NP, and NS genes from other Eurasian influenza viruses. H5N2-R3 viruses contained the HA gene from circulating A(H5N1) clade 2.3.2.1a viruses, NA and M genes from concurrently circulating A(H9N2) influenza viruses, and PB2, PB1, PA, NP, and NS genes from other Eurasian influenza viruses. Representative viruses of all three genotypes and a parental clade 2.3.2.1a strain (H5N1-R0) infected and replicated in mice without prior adaptation; the H5N2-R3 virus replicated to the highest titers in the lung. All viruses efficiently infected and killed chickens. All viruses replicated in inoculated ferrets, but no airborne transmission was detected, and only H5N2-R3 showed limited direct-contact transmission. Our findings demonstrate that although the A(H5N1) viruses circulating in Bangladesh have the capacity to infect and replicate in mammals, they show very limited capacity for transmission. However, reassortment does generate viruses of distinct phenotypes. IMPORTANCE Highly pathogenic avian influenza A(H5N1) viruses have circulated continuously in Bangladesh since 2007, and active surveillance has detected viral evolution driven by mutation and reassortment. Recently, three genetically distinct A(H5N1) reassortant viruses were detected in live poultry markets in Bangladesh. Currently, we cannot assign pandemic risk by only sequencing viruses; it must be conducted empirically. We found that the H5Nx highly pathogenic avian influenza viruses exhibited high virulence in mice and chickens, and one virus had limited capacity to transmit between ferrets, a property considered consistent with a higher zoonotic risk.


2015 ◽  
Vol 21 (5) ◽  
pp. 886-890 ◽  
Author(s):  
Hon S. Ip ◽  
Mia Kim Torchetti ◽  
Rocio Crespo ◽  
Paul Kohrs ◽  
Paul DeBruyn ◽  
...  

2021 ◽  
Author(s):  
Knut Madslien ◽  
Torfinn Moldal ◽  
Britt Gjerset ◽  
Sveinn Gudmundsson ◽  
Arne Follestad ◽  
...  

Abstract Background: Several outbreaks of highly pathogenic avian influenza (HPAI) caused by influenza A virus of subtype H5N8 have been reported in wild birds and poultry in Europe during autumn 2020.Norway is one of the few countries in Europe that had not previously detected HPAI virus, despite widespread active monitoring of both domestic and wild birds since 2005.Results: We report detection of HPAI virus subtype H5N8 in a wild pink-footed goose (Anser brachyrhynchus), and several other geese, ducks and a gull, from south-western Norway in November and December 2020. Despite previous reports of low pathogenic avian influenza (LPAI), this constitutes the first detections of HPAI in Norway.Conclusions: The mode of introduction is unclear, but a northward migration of infected geese or gulls from Denmark or the Netherlands during the autumn of 2020 is currently our main hypothesis for the introduction of HPAI to Norway. Although HPAI of subtype H5N8 has been reported to have very low zoonotic potential, this is a reminder that HPAI with greater zoonotic potential in wild birds may pose a threat in the future.


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