Potential #Pandemic of #H7N9 #Avian #Influenza A Virus in Human (Front Cell Infect Microbiol., abstract)

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

Front Cell Infect Microbiol. 2018 Nov 23;8:414. doi: 10.3389/fcimb.2018.00414. eCollection 2018.

Potential Pandemic of H7N9 Avian Influenza A Virus in Human.

Pu Z1, Xiang D2, Li X1, Luo T1, Shen X1, Murphy RW3, Liao M1,4, Shen Y1,4.

Author information: 1 College of Veterinary Medicine, South China Agricultural University, Guangzhou, China. 2 Joint Influenza Research Centre (SUMC/HKU), Shantou University Medical College, Shantou, China. 3 Centre for Biodiversity and Conservation Biology, Royal Ontario Museum, Toronto, ON, Canada. 4 Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, Guangzhou, China.

 

Abstract

Since 2013, the H7N9 avian influenza A virus (AIV) has caused human infections and to the extent of now surpassing H5N1. This raises an alarm about the potential of H7N9 to become a pandemic problem. Our compilation of the amino acid changes required for AIVs to cross the species-barrier discovers 58 that have very high proportions in both the human- and avian-isolated H7N9 viruses. These changes correspond with sporadic human infections that continue to occur in regions of avian infections. Among the six internal viral genes, amino acid changes do not differ significantly between H9N2 and H7N9, except for V100A in PA, and K526R, D627K, and D701N in PB2. H9N2 AIVs provide internal genes to H7N9. Most of the amino acid changes in H7N9 appear to come directly from H9N2. Seventeen amino acid substitutions appear to have fixed quickly by the 5th wave. Among these, six amino acid sites in HA1 are receptor binding sites, and PB2-A588V was shown to promote the adaptation of AIVs to mammals. The accelerated fixation of mutations may promote the adaptation of H7N9 to human, but need further functional evidence. Although H7N9 AIVs still cannot efficiently transmit between humans, they have the genetic makeup associated with human infections. These viruses must be controlled in poultry to remove the threat of it becoming a human pandemic event.

KEYWORDS: H7N9; avian influenza A virus; genetic marker; host barrier; human infection

PMID: 30533399 PMCID: PMC6265602 DOI: 10.3389/fcimb.2018.00414

Keywords: Avian Influenza; H7N9; Human; Poultry; China.

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#Avian #Influenza A(#H9N2) Virus in #Poultry #Worker, #Pakistan, 2015 (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 1—January 2019 / Dispatch

Avian Influenza A(H9N2) Virus in Poultry Worker, Pakistan, 2015

Muzaffar Ali, Tahir Yaqub, Nadia Mukhtar, Muhammad Imran, Aamir Ghafoor, Muhammad Furqan Shahid, Muhammad Naeem, Munir Iqbal, Gavin J.D. Smith  , and Yvonne C.F. Su

Author affiliations: University of Veterinary and Animal Sciences, Lahore, Pakistan (M. Ali, T. Yaqub, M. Imran, A. Ghafoor, M.F. Shahid); Health Care Department, Government of Punjab, Lahore (N. Mukhtar); Bahauddin Zakariya University, Multan, Pakistan (M. Naeem); The Pirbright Institute, Compton Laboratory, Newbury, UK (M. Iqbal); Duke University, Durham, North Carolina, USA (G.J.D. Smith); Duke-National University Singapore Medical School, Singapore (G.J.D. Smith, Y.C.F. Su)

 

Abstract

Avian influenza A(H9N2) virus isolated from a poultry worker in Pakistan in 2015 was closely related to viruses detected in poultry farms. Observed mutations in the hemagglutinin related to receptor-binding affinity and antigenicity could affect cross-reactivity with prepandemic H9N2 vaccine strains.

Keywords: Avian Influenza; H9N2; Human; Pakistan.

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#Avian #Influenza Virus Subtype #H9N2 Affects #Intestinal #Microbiota, Barrier Structure Injury, and Inflammatory Intestinal Disease in the #Chicken Ileum (Viruses, abstract)

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

Viruses. 2018 May 18;10(5). pii: E270. doi: 10.3390/v10050270.

Avian Influenza Virus Subtype H9N2 Affects Intestinal Microbiota, Barrier Structure Injury, and Inflammatory Intestinal Disease in the Chicken Ileum.

Li H1,2,3,4, Liu X5,6,7,8, Chen F9,10,11,12, Zuo K13, Wu C14,15,16,17,18, Yan Y19,20,21,22, Chen W23,24,25,26,27, Lin W28,29,30,31,32, Xie Q33,34,35,36,37.

Author information: 1 College of Animal Science, South China Agricultural University, Guangzhou 510642, China. dongkeoffice@scau.edu.cn. 2 Key Laboratory of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, Guangzhou 510642, China. dongkeoffice@scau.edu.cn. 3 Key Laboratory of Animal Health Aquaculture and Environmental Control, Guangdong, Guangzhou 510642, China. dongkeoffice@scau.edu.cn. 4 Guangdong Provincial Key Laboratory of Agro-Animal Genomics and Molecular Breeding, Guangzhou 510642, China. dongkeoffice@scau.edu.cn. 5 College of Animal Science, South China Agricultural University, Guangzhou 510642, China. fky19842004@163.com. 6 Key Laboratory of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, Guangzhou 510642, China. fky19842004@163.com. 7 Key Laboratory of Animal Health Aquaculture and Environmental Control, Guangdong, Guangzhou 510642, China. fky19842004@163.com. 8 Guangdong Provincial Key Laboratory of Agro-Animal Genomics and Molecular Breeding, Guangzhou 510642, China. fky19842004@163.com. 9 College of Animal Science, South China Agricultural University, Guangzhou 510642, China. cfy329@scau.edu.cn. 10 Key Laboratory of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, Guangzhou 510642, China. cfy329@scau.edu.cn. 11 Key Laboratory of Animal Health Aquaculture and Environmental Control, Guangdong, Guangzhou 510642, China. cfy329@scau.edu.cn. 12 Guangdong Provincial Key Laboratory of Agro-Animal Genomics and Molecular Breeding, Guangzhou 510642, China. cfy329@scau.edu.cn. 13 Veterinary Laboratory, Guangzhou Zoo, Guangzhou 510642, China. hnlhxin@126.com. 14 College of Animal Science, South China Agricultural University, Guangzhou 510642, China. che.w@foxmail.com. 15 Key Laboratory of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, Guangzhou 510642, China. che.w@foxmail.com. 16 Key Laboratory of Animal Health Aquaculture and Environmental Control, Guangdong, Guangzhou 510642, China. che.w@foxmail.com. 17 Guangdong Provincial Key Laboratory of Agro-Animal Genomics and Molecular Breeding, Guangzhou 510642, China. che.w@foxmail.com. 18 South China Collaborative Innovation Center for Poultry Disease Control and Product Safety, Guangzhou 510642, China. che.w@foxmail.com. 19 College of Animal Science, South China Agricultural University, Guangzhou 510642, China. liaozhihong@163.com. 20 Key Laboratory of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, Guangzhou 510642, China. liaozhihong@163.com. 21 Key Laboratory of Animal Health Aquaculture and Environmental Control, Guangdong, Guangzhou 510642, China. liaozhihong@163.com. 22 Guangdong Provincial Key Laboratory of Agro-Animal Genomics and Molecular Breeding, Guangzhou 510642, China. liaozhihong@163.com. 23 College of Animal Science, South China Agricultural University, Guangzhou 510642, China. wgchen81@scau.edu.cn.24 Key Laboratory of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, Guangzhou 510642, China. wgchen81@scau.edu.cn. 25 Key Laboratory of Animal Health Aquaculture and Environmental Control, Guangdong, Guangzhou 510642, China. wgchen81@scau.edu.cn. 26 Guangdong Provincial Key Laboratory of Agro-Animal Genomics and Molecular Breeding, Guangzhou 510642, China. wgchen81@scau.edu.cn. 27 South China Collaborative Innovation Center for Poultry Disease Control and Product Safety, Guangzhou 510642, China. wgchen81@scau.edu.cn. 28 College of Animal Science, South China Agricultural University, Guangzhou 510642, China. wenchenglin@scau.edu.cn. 29 Key Laboratory of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, Guangzhou 510642, China. wenchenglin@scau.edu.cn. 30 Key Laboratory of Animal Health Aquaculture and Environmental Control, Guangdong, Guangzhou 510642, China. wenchenglin@scau.edu.cn. 31 Guangdong Provincial Key Laboratory of Agro-Animal Genomics and Molecular Breeding, Guangzhou 510642, China. wenchenglin@scau.edu.cn. 32 South China Collaborative Innovation Center for Poultry Disease Control and Product Safety, Guangzhou 510642, China. wenchenglin@scau.edu.cn. 33 College of Animal Science, South China Agricultural University, Guangzhou 510642, China. qmx@scau.edu.cn. 34 Key Laboratory of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, Guangzhou 510642, China. qmx@scau.edu.cn. 35 Key Laboratory of Animal Health Aquaculture and Environmental Control, Guangdong, Guangzhou 510642, China. qmx@scau.edu.cn. 36 Guangdong Provincial Key Laboratory of Agro-Animal Genomics and Molecular Breeding, Guangzhou 510642, China. qmx@scau.edu.cn. 37 South China Collaborative Innovation Center for Poultry Disease Control and Product Safety, Guangzhou 510642, China. qmx@scau.edu.cn.

 

Abstract

Avian influenza virus subtype H9N2 (H9N2 AIV) has caused significant losses to the poultry industry due to the high mortality associated with secondary infections attributable to E. coli. This study tries to address the underlying secondary mechanisms after H9N2 AIV infection. Initially, nine day-old specific pathogen-free chickens were assigned to control (uninfected) and H9N2-infected groups, respectively. Using Illumina sequencing, histological examination, and quantitative real-time PCR, it was found that H9N2 AIV caused intestinal microbiota disorder, injury, and inflammatory damage to the intestinal mucosa. Notably, the genera Escherichia, especially E. coli, significantly increased (p < 0.01) at five days post-infection (dpi), while Lactobacillus, Enterococcus, and other probiotic organisms were significantly reduced (p < 0.01). Simultaneously, the mRNA expression of tight junction proteins (ZO-1, claudin 3, and occludin), TFF2, and Muc2 were significantly reduced (p < 0.01), indicating the destruction of the intestinal epithelial cell tight junctions and the damage of mucin layer construction. Moreover, the mRNA expression of proinflammatory cytokines IFN-γ, IL-22, IFN-α, and IL-17A in intestinal epithelial cells were significantly upregulated, resulting in the inflammatory response and intestinal injury. Our findings may provide a theoretical basis for observed gastroenteritis-like symptoms such as diarrhea and secondary E. coli infection following H9N2 AIV infection.

KEYWORDS: E. coli; H9N2 AIV; barrier injury; inflammatory intestinal disease; intestinal microbiota

PMID: 29783653 PMCID: PMC5977263 DOI: 10.3390/v10050270 [Indexed for MEDLINE]  Free PMC Article

Keywords: Avian Influenza, H9N2; Poultry.

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Molecular #evolutionary and #antigenic characteristics of newly isolated #H9N2 #avian #influenza viruses in #Guangdong province, #China (Arch Virol., abstract)

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

Arch Virol. 2018 Nov 24. doi: 10.1007/s00705-018-4103-4. [Epub ahead of print]

Molecular evolutionary and antigenic characteristics of newly isolated H9N2 avian influenza viruses in Guangdong province, China.

Zhang J1, Wu H1, Zhang Y1, Cao M1, Brisse M2, Zhu W1,2, Li R1, Liu M1, Cai M3, Chen J4, Chen J5.

Author information: 1 School of Life Science and Engineering, Foshan University, Foshan, 528000, Guangdong, People’s Republic of China. 2 College of Veterinary Medicine, University of Minnesota, Twin Cites Campus, Saint Paul, MN, 55108, USA. 3 Department of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Science, Guangzhou Medical University, Xinzao Town, Panyu, Guangzhou, 511436, Guangdong, People’s Republic of China. 4 School of Life Science and Engineering, Foshan University, Foshan, 528000, Guangdong, People’s Republic of China. jianhongchen2012@126.com. 5 School of Life Science and Engineering, Foshan University, Foshan, 528000, Guangdong, People’s Republic of China. jidangchen@fosu.edu.cn.

 

Abstract

Four new H9N2 avian influenza viruses (AIVs) were isolated from domestic birds in Guangdong between December 2015 and April 2016. Nucleotide sequence comparisons indicated that most of the internal genes of these four strains were highly similar to those of human H7N9 viruses. Amino acid substitutions and deletions found in the HA and NA proteins indicated that all four of these new isolates may have an enhanced ability to infect humans and other mammals. A cross-hemagglutinin-inhibition assay, conducted with two vaccine strains that are broadly used in China, suggested that antisera against vaccine candidates could not provide complete inhibition of the new isolates.

PMID: 30474753 DOI: 10.1007/s00705-018-4103-4

Keywords: A/H9N2; Avian Influenza; Reassortant Strains; Poultry; Guangdong; China.

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#Genetic #compatibility of #reassortants between #avian #H5N1 and #H9N2 #influenza viruses with higher pathogenicity in #mammals (J Virol., abstract)

[Source: Journal of Virology, full page: (LINK). Abstract, edited.]

Genetic compatibility of reassortants between avian H5N1 and H9N2 influenza viruses with higher pathogenicity in mammals

Yasuha Arai, Madiha S. Ibrahim, Emad M. Elgendy, Tomo Daidoji, Takao Ono, Yasuo Suzuki, Takaaki Nakaya, Kazuhiko Matsumoto, Yohei Watanabe

DOI: 10.1128/JVI.01969-18

 

ABSTRACT

The co-circulation of H5N1 and H9N2 avian influenza viruses in birds in Egypt provides reassortment opportunities between these two viruses. However, little is known about the emergence potential of reassortants derived from Egyptian H5N1 and H9N2 viruses and about the biological properties of such reassortants. To evaluate the potential public health risk of reassortants of these viruses, we used reverse genetics to generate the 63 possible reassortants derived from contemporary Egyptian H5N1 and H9N2 viruses, containing the H5N1 surface gene segments and combinations of the H5N1 and H9N2 internal gene segments, and analyzed their genetic compatibility, replication ability and virulence in mice. Genes in the reassortants showed remarkably high compatibility. Replication of most reassortants was higher than the parental H5N1 virus in human cells. Six reassortants were thought to emerge in birds under neutral or positive selective pressure, and four of them had higher pathogenicity in vivo than the parental H5N1 and H9N2 viruses. Our results indicated that H5N1-H9N2 reassortants could be transmitted efficiently to mammals with significant public health risk if they emerge in Egypt, although the viruses might not emerge frequently in birds.

 

IMPORTANCE

Close interaction between avian influenza (AI) viruses and humans in Egypt appears to have resulted in many of the worldwide cases of human infections by both H5N1 and H9N2 AI viruses. Egypt is regarded as a hot spot of AI virus evolution. Although no natural reassortant of H5N1 and H9N2 AI viruses has been reported so far, their co-circulation in Egypt may allow emergence of reassortants that may present a significant public health risk. Using reverse genetics, we report here the first comprehensive data showing that H5N1-N9N2 reassortants have fairly high genetic compatibility and possibly higher pathogenicity in mammals, including humans, than the parental viruses. Our results provide insight into the emergence potential of avian H5N1-H9N2 reassortants that may pose a high public health risk.

Copyright © 2018 Arai et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license.

Keywords: Avian Influenza; H5N1; H9N2; Reassortant strains.

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High frequency of #reassortment after #coinfection of #chickens with the #H4N6 and #H9N2 #influenza A viruses and the biological characteristics of the reassortants (Vet Microbiol., abstract)

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

Vet Microbiol. 2018 Aug;222:11-17. doi: 10.1016/j.vetmic.2018.06.011. Epub 2018 Jun 18.

High frequency of reassortment after co-infection of chickens with the H4N6 and H9N2 influenza A viruses and the biological characteristics of the reassortants.

Li X1, Liu B2, Ma S3, Cui P3, Liu W4, Li Y4, Guo J5, Chen H6.

Author information: 1 College of Agricultural, Liaocheng University, Liaocheng, People’s Republic of China. Electronic address: lixuyong@lcu.edu.cn. 2 College of veterinary medicine, Qingdao Agricultural University, Qingdao, People’s Republic of China. 3 State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, CAAS, People’s Republic of China. 4 College of Agricultural, Liaocheng University, Liaocheng, People’s Republic of China. 5 College of Agricultural, Liaocheng University, Liaocheng, People’s Republic of China. Electronic address: guojing@lcu.edu.cn. 6 State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, CAAS, People’s Republic of China. Electronic address: chenhualan@caas.cn.

 

Abstract

H4 and H9 avian influenza viruses (AIVs) are two of the most prevalent influenza viruses worldwide. The co-existence of H4 and H9 viruses in multiple avian species provides an opportunity for the generation of novel reassortants and for viral evolution. The diversity of the biological characteristics of the reassortants enhances the potential threat to the poultry industry and to public health. To evaluate the reassortment of these viruses and the potential public risk of the reassortants, we co-infected chickens with H4N6 and H9N2 viruses derived from poultry and tested the replication and virulence of the reassortant viruses in mice. A high frequency of reassortment was detected in chickens after co-infection with these two viruses and nine reassortants of six genotypes were purified from the chicken samples. Two H9N2 reassortants containing the PA of the parent H4N6 virus showed higher virulence than the parent H9N2 virus, revealing the significant role of the H4N6 wt virus PA gene in viral reassortment. Analysis of the polymerase activity of the ribonucleoprotein (RNP) complex in vitro suggested that the PA of H4N6 wt origin enhanced polymerase activity. Our results indicate that co-infection of an avian individual with the H4N6 and H9N2 viruses leads to a high frequency of reassortment and generates some reassortants that have higher virulence than the wild-type viruses in mammals. These results highlight the potential public risk of the avian influenza reassortants and the importance of surveillance of the co-existence of the H4N6 and H9N2 viruses in avian species and other animals.

KEYWORDS: Chicken; Co-infection; H4N6; H9N2; Mice; Reassortants

PMID: 30080665 DOI: 10.1016/j.vetmic.2018.06.011 [Indexed for MEDLINE]

Keywords: Avian Influenza; H4N6; H9N2; Reassortant Strain; Poultry.

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Association of Increased #Receptor-Binding Avidity of #Influenza A(#H9N2) Viruses with Escape from #Antibody-Based Immunity and Enhanced #Zoonotic Potential (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 1—January 2019 / Research

Association of Increased Receptor-Binding Avidity of Influenza A(H9N2) Viruses with Escape from Antibody-Based Immunity and Enhanced Zoonotic Potential

Joshua E. Sealy, Tahir Yaqub, Thomas P. Peacock1, Pengxiang Chang, Burcu Ermetal, Anabel Clements, Jean-Remy Sadeyen, Arslan Mehboob2, Holly Shelton, Juliet E. Bryant, Rod S. Daniels, John W. McCauley, Munir Iqbal, and Jean-Remy

Author affiliations: The Pirbright Institute, Pirbright, UK (J.E. Sealy, T.P. Peacock, P. Chang, A. Clements, J.-R. Sadeyen, H. Shelton, M. Iqbal); University of Veterinary and Animal Sciences, Lahore, Pakistan (T. Yaqub, A. Mehboob); The Francis Crick Institute, London (B. Ermetal, R.S. Daniels, J.W. McCauley); Fondation Mérieux, Lyon, France (J.E. Bryant)

Abstract

We characterized 55 influenza A(H9N2) viruses isolated in Pakistan during 2014–2016 and found that the hemagglutinin gene is of the G1 lineage and that internal genes have differentiated into a variety of novel genotypes. Some isolates had up to 4-fold reduction in hemagglutination inhibition titers compared with older viruses. Viruses with hemagglutinin A180T/V substitutions conveyed this antigenic diversity and also caused up to 3,500-fold greater binding to avian-like and >20-fold greater binding to human-like sialic acid receptor analogs. This enhanced binding avidity led to reduced virus replication in primary and continuous cell culture. We confirmed that altered receptor-binding avidity of H9N2 viruses, including enhanced binding to human-like receptors, results in antigenic variation in avian influenza viruses. Consequently, current vaccine formulations might not induce adequate protective immunity in poultry, and emergence of isolates with marked avidity for human-like receptors increases the zoonotic risk.

Keywords: Avian Influenza; H9N2; Pakistan.

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