Direct #evidence of #H7N7 #avian #influenza virus #mutation from low to high virulence on a single #poultry premises during an #outbreak in free range chickens in the #UK, 2008 (Infect Genet Evol., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Infect Genet Evol. 2018 Oct;64:13-31. doi: 10.1016/j.meegid.2018.06.005. Epub 2018 Jun 5.

Direct evidence of H7N7 avian influenza virus mutation from low to high virulence on a single poultry premises during an outbreak in free range chickens in the UK, 2008.

Seekings AH1, Slomka MJ2, Russell C2, Howard WA2, Choudhury B2, Nuñéz A3, Löndt BZ2, Cox W2, Ceeraz V2, Thorén P4, Irvine RM2, Manvell RJ2, Banks J2, Brown IH2.

Author information: 1 Virology Department, Animal and Plant Health Agency (APHA-Weybridge), Addlestone, Surrey KT15 3NB, United Kingdom. Electronic address: amanda.seekings@apha.gsi.gov.uk. 2 Virology Department, Animal and Plant Health Agency (APHA-Weybridge), Addlestone, Surrey KT15 3NB, United Kingdom. 3 Pathology Department, Animal and Plant Health Agency (APHA-Weybridge), Addlestone, Surrey KT15 3NB, United Kingdom. 4 Swedish Agricultural University (SLU), Uppsala, Sweden.

 

Abstract

H5 and H7 subtypes of low pathogenicity avian influenza viruses (LPAIVs) have the potential to evolve into highly pathogenic avian influenza viruses (HPAIVs), causing high mortality in galliforme poultry with substantial economic losses for the poultry industry. This study provides direct evidence of H7N7 LPAIV mutation to HPAIV on a single poultry premises during an outbreak that occurred in June 2008 in free range laying hens in Oxfordshire, UK. We report the first detection of a rare di-basic cleavage site (CS) motif (PEIPKKRGLF), unique to galliformes, that has previously been associated with a LPAIV phenotype. Three distinct HPAIV CS sequences (PEIPKRKKRGLF, PEIPKKKKRGLF and PEIPKKKKKKRGLF) were identified in the infected sheds suggesting molecular evolution at the outbreak premises. Further evidence for H7N7 LPAIV preceding mutation to HPAIV was derived by examining clinical signs, epidemiological descriptions and analysing laboratory results on the timing and proportions of seroconversion and virus shedding at each infected shed on the premises. In addition to describing how the outbreak was diagnosed and managed via statutory laboratory testing, phylogenetic analysis revealed reassortant events during 2006-2008 that suggested likely incursion of a wild bird origin LPAIV precursor to the H7N7 HPAIV outbreak. Identifying a precursor LPAIV is important for understanding the molecular changes and mechanisms involved in the emergence of HPAIV. This information can lead to understanding how and why only some H7 LPAIVs appear to readily mutate to HPAIV.

Crown Copyright © 2018. Published by Elsevier B.V. All rights reserved.

KEYWORDS: Avian influenza; H7N7; HPAIV; Pathogenicity

PMID: 29883773 DOI: 10.1016/j.meegid.2018.06.005 [Indexed for MEDLINE]

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Keywords: Avian Influenza; H7N7; Poultry; UK.

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#Isolation of highly pathogenic #H5N6 #avian #influenza virus in Southern #Vietnam with #genetic similarity to those infecting #humans in #China (Transbound Emerg Dis., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Transbound Emerg Dis. 2019 Jul 15. doi: 10.1111/tbed.13294. [Epub ahead of print]

Isolation of highly pathogenic H5N6 avian influenza virus in Southern Vietnam with genetic similarity to those infecting humans in China.

Tsunekuni R1,2, Sudo K3, Nguyen PT4, Luu BD4, Phuong TD4, Tan TM4, Tung N5, Mine J1,2, Nakayama M1,2, Tanikawa T1,2, Sharshov K6, Takemae N1,2, Saito T1,2,7.

Author information: 1 Division of Transboundary Animal Disease, National Institute of Animal Health, NARO, Tsukuba, Japan. 2 Thailand-Japan Zoonotic Diseases Collaboration Center, Bangkok, Thailand. 3 National Veterinary Assay Laboratory, Ministry of Agriculture, Forestry and Fisheries, Japan. 4 Regional Animal Health Office No. 6, Department of Animal Health, Vietnam. 5 Division of International Cooperation and Communications, Department of Animal Health, Hanoi, Vietnam. 6 Federal Research Center of Fundamental and Translational Medicine, Novosibirsk, Russia. 7 United Graduate School of Veterinary Sciences, Gifu University, Japan.

 

Abstract

Since 2013, H5N6 highly pathogenic avian influenza viruses (HPAIVs) have been responsible for outbreaks in poultry and wild birds around Asia. H5N6 HPAIV is also a public concern due to sporadic human infections being reported in China. In the current study, we isolated an H5N6 HPAIV strain (A/Muscovy duck/Long An/AI470/2018; AI470) from an outbreak at a Muscovy duck farm in Long An Province in Southern Vietnam in July 2018 and genetically characterized it. Basic Local Alignment Search Tool (BLAST) analysis revealed that the eight genomic segments of AI470 were most closely related (99.6-99.9%) to A/common gull/Saratov/1676/2018 (H5N6), which was isolated in October 2018 in Russia. Furthermore, AI470 also shared 99.4-99.9% homology with A/Guangxi/32797/2018, an H5N6 HPAIV strain that infected humans in China in 2018. Phylogenetic analyses of the entire genome showed that AI470 was directly derived from H5N6 HPAIVs that were in South China from 2015 to 2018 and clustered with four H5N6 HPAIV strains of human origin in South China from 2017 to 2018. This indicated that AI470 was introduced into Vietnam from China. In addition, molecular characteristics related to mammalian adaptation among the recent human H5N6 HPAIV viruses, except PB2 E627K, were shared by AI470. These findings are cause for concern since H5N6 HPAIV strains that possess a risk of human infection have crossed the Chinese border.

This article is protected by copyright. All rights reserved.

KEYWORDS: G1.1; Highly pathogenic avian influenza virus; South China; Vietnam; human infection

PMID: 31309743 DOI: 10.1111/tbed.13294

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Keywords: Avian Influenza; H5N6; Poultry; Vietnam.

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Characterization of viral #genomic #mutations in novel #influenza A (#H7N9)-infected #patients: the association between #oseltamivir-resistant variants and viral shedding duration (Virus Genes., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Virus Genes. 2019 Jul 13. doi: 10.1007/s11262-019-01678-8. [Epub ahead of print]

Characterization of viral genomic mutations in novel influenza A (H7N9)-infected patients: the association between oseltamivir-resistant variants and viral shedding duration.

Chen R1, Zou Q2,3, Xie G2,3, Yu F2,3, Yang X2,3, Cao L1, Huo Z4, Zheng S5,6.

Author information: 1 Zhejiang Chinese Medical University, Hangzhou, People’s Republic of China. 2 Center of Clinical Laboratory, First Affiliated Hospital, School of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou, 310003, People’s Republic of China. 3 Key Laboratory of Clinical In Vitro Diagnostic Techniques of Zhejiang Province, Hangzhou, People’s Republic of China. 4 Experimental Teaching Center, School of Basic Medical Sciences, Zhejiang University, 866 Yuhangtang Road, Hangzhou, 310058, People’s Republic of China. zxhuo@zju.edu.cn. 5 Center of Clinical Laboratory, First Affiliated Hospital, School of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou, 310003, People’s Republic of China. zsfzheng@zju.edu.cn. 6 Key Laboratory of Clinical In Vitro Diagnostic Techniques of Zhejiang Province, Hangzhou, People’s Republic of China. zsfzheng@zju.edu.cn.

 

Abstract

Since February 2013, human infections with the novel influenza A H7N9 virus have occurred in eastern China. It is important to detect mutations in viral genes and analyze the clinical features of patients and viral shedding duration related to neuraminidase inhibitor (NAI) resistance. We collected clinical specimens from 31 hospitalized H7N9 patients and sequenced NA, PB2, HA, and M gene fragments. Of the 31 identified patients, 7 (22.6%) carried the R292K substitution in NA, 30 (96.8%), 3 (9.7%), and 5 (16.1%) carried E627K, Q591K, and D701N mutations in PB2, respectively, and 2 (6.5%) carried both E627K and D701N mutations in PB2. All 26 identified patients harbored Q226L mutations and possessed only a single arginine (R) at cleavage sites in the HA and a S31N mutation in M2. Among 7 NA-R292K mutated patients, 3 died and 4 were discharged. There was no significant difference in the days that patients started oseltamivir treatment after symptom onset between NA-R292K mutant and NA-R292 wild-type patients (median days, 7 vs 6, P = 0.374). NA-R292K mutant patients had a significantly longer duration of viral shedding than NA-R292 wild-type patients after oseltamivir treatment (median days, 10 vs 5, P = 0.022). The mutation of R292K in NA conferring the potential ability of oseltamivir resistance resulted in prolonged viral duration and poor outcome and should be taken into consideration in the clinical management of infected patients.

KEYWORDS: Influenza A (H7N9); Mutation; Neuraminidase (NA); Oseltamivir resistance; Viral duration

PMID: 31302878 DOI: 10.1007/s11262-019-01678-8

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Keywords: Avian Influenza; H7N9; Antivirals; Drugs Resistance; Oseltamivir; China; Human.

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Emergence of #Influenza A(#H7N4) Virus, #Cambodia (Emerg Infect Dis., abstract)

[Source: US Centers for Disease Control and Prevention (CDC), Emerging Infectious Diseases Journal, full page: (LINK). Abstract, edited.]

Volume 25, Number 10—October 2019 / Research Letter

Emergence of Influenza A(H7N4) Virus, Cambodia

Dhanasekaran Vijaykrishna, Yi-Mo Deng, Miguel L. Grau, Matthew Kay, Annika Suttie, Paul F. Horwood, Wantanee Kalpravidh, Filip Claes, Kristina Osbjer, Phillipe Dussart, Ian G. Barr, and Erik A. Karlsson

Author affiliations: Peter Doherty Institute for Infection and Immunity, Melbourne, Victoria, Australia (D. Vijaykrishna, Y.-M. Deng, M. Kay, I.G. Barr); Monash University, Melbourne (D. Vijaykrishna, M.L. Grau); Institut Pasteur du Cambodge, Phnom Penh, Cambodia (A. Suttie, P.F. Horwood, P. Dussart, E.A. Karlsson); James Cook University, Townsville, Queensland, Australia (P.F. Horwood); Food and Agriculture Organization of the United Nations, Bangkok, Thailand (W. Kalpravidh, F. Claes); Food and Agriculture Organization of the United Nations, Phnom Penh, Cambodia (K. Osbjer)

 

Abstract

Active surveillance in high-risk sites in Cambodia has identified multiple low-pathogenicity influenza A(H7) viruses, mainly in ducks. None fall within the A/Anhui/1/2013(H7N9) lineage; however, some A(H7) viruses from 2018 show temporal and phylogenetic similarity to the H7N4 virus that caused a nonfatal infection in Jiangsu Province, China, in December 2017.

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Keywords: Avian Influenza; H7N4; Reassortant strain; Cambodia.

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Circulation, #Evolution and #Transmission of Highly Pathogenic #Avian #Influenza A (#H5N8) virus, 2016-2018 (J Infect., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

J Infect. 2019 Jul 12. pii: S0163-4453(19)30214-2. doi: 10.1016/j.jinf.2019.07.005. [Epub ahead of print]

Circulation, Evolution and Transmission of Highly Pathogenic Avian Influenza A (H5N8) virus, 2016-2018.

Chen J1, Liang B2, Hu J3, Liu H3, Sun J4, Li M5, Chen Q6, He Y4, Liu D7.

Author information: 1 CAS Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China; National Virus Resource Center, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China; Center for Influenza Research and Early warning (CASCIRE), Chinese Academy of Sciences, Beijing, 100101, China. Electronic address: chenjj@wh.iov.cn. 2 CAS Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China; National Virus Resource Center, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China; University of Chinese Academy Sciences, Beijing, 101409, China. 3 CAS Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China; National Virus Resource Center, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China. 4 Qinghai Lake National Nature Reserve, Xining, 810099, China. 5 CAS Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China. 6 CAS Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China; Center for Influenza Research and Early warning (CASCIRE), Chinese Academy of Sciences, Beijing, 100101, China. 7 CAS Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China; National Virus Resource Center, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China; Center for Influenza Research and Early warning (CASCIRE), Chinese Academy of Sciences, Beijing, 100101, China; University of Chinese Academy Sciences, Beijing, 101409, China. Electronic address: liud@wh.iov.cn.

 

Abstract

OBJECTIVES:

A second wave of highly pathogenic avian influenza A virus (HPAIV) H5N8 clade 2.3.4.4 has spread globally, causing outbreaks among wild birds and domestic poultry since autumn 2016. The circulation and evolutionary dynamics of the virus remain largely unknown.

METHODS:

We performed surveillance for H5N8 in Qinghai Lake in China since the emergence of the virus (from 2016 to 2018). By analyzing recovered viruses in Qinghai Lake and all related viruses worldwide (449 strains), we identified the genotypes, estimated their genesis and reassortment, and evaluated their global distribution and transmission.

RESULTS:

Through surveillance of wild migratory birds around Qinghai Lake between 2016 and 2018, we revealed that the H5N8 was introduced into Qinghai Lake bird populations (QH-H5N8), with distinct gene constellations in 2016 and 2017. A global analysis of QH-H5N8-related viruses showed that avian influenza viruses with low pathogenicity in wild birds contributed to the high diversity of genotypes; the major reassortment events possibly occurred during the 2016 breeding season and the following winters.

CONCLUSIONS:

Continued circulation of QH-H5N8-related viruses among wild birds has resulted in the global distribution of high genotypic diversity. Thus, these viruses pose an ongoing threat to wild and domestic bird populations and warrant continuous surveillance.

Copyright © 2019. Published by Elsevier Ltd.

KEYWORDS: Circulation; Evolution; H5N8 avian influenza; Migratory birds; Transmission

PMID: 31306679 DOI: 10.1016/j.jinf.2019.07.005

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Keywords: Avian Influenza; H5N8; Poultry; Wild Birds.

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Prevailing I292V #PB2 #mutation in #avian #influenza #H9N2 virus increases viral #polymerase function and attenuates IFN-β induction in human cells (J Gen Virol., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

J Gen Virol. 2019 Jul 15. doi: 10.1099/jgv.0.001294. [Epub ahead of print]

Prevailing I292V PB2 mutation in avian influenza H9N2 virus increases viral polymerase function and attenuates IFN-β induction in human cells.

Gao W1, Zu Z1, Liu J1, Song J1, Wang X1, Wang C1, Liu L1, Tong Q1, Wang M1, Sun H1, Sun Y1, Liu J1, Chang KC2, Pu J1.

Author information: 1 Key Laboratory of Animal Epidemiology, Ministry of Agriculture, College of Veterinary Medicine, China Agricultural University, Beijing, 100193, PR China. 2 School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington Campus, Loughborough, UK.

 

Abstract

Adaptation of PB2 protein is important for the establishment of avian influenza viruses in mammalian hosts. Here, we identify I292V as the prevalent mutation in PB2 of circulating avian H9N2 and pandemic H1N1 viruses. The same dominant PB2 mutation is also found in most human isolates of emergent avian H7N9 and H10N8 viruses. In human cells, PB2-292V in H9N2 virus has the combined ability of conferring higher viral polymerase activity and stronger attenuation of IFN-β induction than that of its predecessor PB2-292I. IFN-β attenuation is accompanied by higher binding affinity of PB2-292V for host mitochondrial antiviral signalling protein, an important intermediary protein in the induction of IFN-β. In the mouse in vivo model, PB2-292V mutation increases H9N2 virus replication with ensuing increase in disease severity. Collectively, PB2-292V is a new mammalian adaptive marker that promotes H9N2 virus replication in mammalian hosts with the potential to improve transmission from birds to humans.

PMID: 31305236 DOI: 10.1099/jgv.0.001294

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Keywords: Avian Influenza; H9N2; Viral pathogenesis.

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#Respiratory disease due to mixed viral #infections in #poultry flocks in #Egypt between 2017 and 2018: #Upsurge of highly pathogenic #avian #influenza virus subtype #H5N8 since 2018 (Transbound Emerg Dis., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Transbound Emerg Dis. 2019 Jul 11. doi: 10.1111/tbed.13281. [Epub ahead of print]

Respiratory disease due to mixed viral infections in poultry flocks in Egypt between 2017 and 2018: Upsurge of highly pathogenic avian influenza virus subtype H5N8 since 2018.

Hassan KE1,2, El-Kady MF2, El-Sawah AAA2, Luttermann C3, Parvin R1,4, Shany S2, Beer M1, Harder T1.

Author information: 1 Institute of Diagnostic Virology, Friedrich-Loeffler-Institute, Greifswald-Riems, Germany. 2 Department of Poultry Diseases, Faculty of Veterinary Medicine, Beni-Suef University, Beni-Suef, Egypt. 3 Institute of Immunology Virology, Friedrich-Loeffler-Institute, Greifswald-Riems, Germany. 4 Department of Pathology, Faculty of Veterinary Science, Bangladesh Agricultural University, Mymensingh, Bangladesh.

 

Abstract

For several years, poultry production in Egypt has been suffering from co-circulation of multiple respiratory viruses including highly pathogenic avian influenza virus (HPAIV) H5N1 (clade 2.2.1.2) and low pathogenic H9N2 (clade G1-B). Incursion of HPAIV H5N8 (clade 2.3.4.4b) to Egypt in November 2016 via wild birds followed by spread into commercial poultry flocks further complicated the situation. Current analyses focussed on 39 poultry farms suffering from respiratory manifestation and high mortality in six Egyptian governorates during 2017-2018. Real-time RT-PCR (RT-qPCR) substantiated the co-presence of at least two respiratory virus species in more than 80% of the investigated flocks. The percentage of HPAIV H5N1-positive holdings was fairly stable in 2017 (12.8%) and 2018 (10.2%), while the percentage of HPAIV H5N8-positive holdings increased from 23% in 2017 to 66.6% during 2018. The proportion of H9N2-positive samples was constantly high (2017:100% and 2018:63%), and H9N2 co-circulated with HPAIV H5N8 in 22 out of 39 (56.8%) flocks. Analyses of 26 H5, 18 H9 and 4 N2 new sequences confirmed continuous genetic diversification. In silico analysis revealed numerous amino acid substitutions in the HA and NA proteins suggestive of increased adaptation to mammalian hosts and putative antigenic variation. For sensitive detection of H9N2 viruses by RT-qPCR, an update of primers and probe sequences was crucial. Reasons for the relative increase of HPAIV H5N8 infections versus H5N1 remained unclear, but lack of suitable vaccines against clade 2.3.4.4b cannot be excluded. A reconsideration of surveillance and control measures should include updating of diagnostic tools and vaccination strategies.

© 2019 Blackwell Verlag GmbH.

KEYWORDS: Egypt; Highly pathogenic avian influenza; co-infection; control; diagnostic tools; reassortant viruses

PMID: 31297991 DOI: 10.1111/tbed.13281

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Keywords: Avian Influenza; H5N1; H5N8; H9N2; Poultry; Egypt.

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