#Epidemiological and molecular analysis of #avian #influenza A(#H7N9) virus in #Shanghai, #China, 2013-2017 (Infect Drug Resist., abstract)

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

Infect Drug Resist. 2018 Nov 22;11:2411-2424. doi: 10.2147/IDR.S179517. eCollection 2018.

Epidemiological and molecular analysis of avian influenza A(H7N9) virus in Shanghai, China, 2013-2017.

Wang SJ1,2,3, Liu XW1, Shen X1,2, Hua XG1,2, Cui L1,2.

Author information: 1 Department of Animal Science, Shanghai Key Laboratory of Veterinary Biotechnology, Shanghai Jiao Tong University, Shanghai 200240, China, lcui@sjtu.edu.cn. 2 Department of Animal Science, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai 200240, China, lcui@sjtu.edu.cn. 3 Animal and Plant Quarantine Agency, Gimcheon 39660, Republic of Korea.




Human infections with a novel avian influenza A virus (H7N9) were reported in Shanghai municipality, China, at the beginning of 2013. High-pathogenic avian influenza (HPAI) H7N9 virus emerged in late February 2017 along with existing low-pathogenic avian influenza (LPAI) H7N9 virus, and this has the potential to develop into a pandemic that could be harmful to humans.


To elucidate the epidemiological characteristics of H7N9-infected cases from 2013 to 2017 in Shanghai, data on the 59 laboratory-confirmed human cases and 26 bird and environmental contamination cases were collected from the WHO website and Food and Agriculture Organization Emergency Prevention System for Animal Health (FAO EMPRES-AH). Full-length sequences of H7N9 viruses that emerged in Shanghai were collected from the Global Initiative on Sharing Avian Influenza Data to analyze the evolutionary and genetic features.


We found that genetically different strains emerged in every epidemic in Shanghai, and most of the circulating H7N9 strains had affinity to human-type receptors, with the characteristics of high-virulence and low-pathogenic influenza viruses. Furthermore, our findings suggest that the Shanghai chicken strains are closely related to the HPAI H7N9 virus A/Guangdong/17SF003/2016, indicating that this viral strain is of avian origin and generated from the LPAI H7N9 viruses in Shanghai. The gradual decrease in H7N9 human infection in Shanghai was probably due to the control measures taken by the Shanghai government and the enhanced public awareness leading to a reduced risk of H7N9 virus infection. However, LPAI H7N9 viruses from poultry and environmental samples were continually detected in Shanghai across the epidemics, increasing the risk of new emerging H7N9 outbreaks.


It is important to consistently obtain sufficient surveillance data and implement prevention measures against H7N9 viruses in Shanghai municipality.

KEYWORDS: H7N9 virus; epidemiology; molecular evolutionary study; phylogenetic tree

PMID: 30538508 PMCID: PMC6254586 DOI: 10.2147/IDR.S179517

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



#Pathogenicity of two novel #human-origin #H7N9 highly pathogenic #avian #influenza viruses in #chickens and #ducks (Arch Virol., abstract)

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

Arch Virol. 2018 Dec 11. doi: 10.1007/s00705-018-4102-5. [Epub ahead of print]

Pathogenicity of two novel human-origin H7N9 highly pathogenic avian influenza viruses in chickens and ducks.

Tanikawa T1, Uchida Y1, Takemae N1, Tsunekuni R1, Mine J1, Liu MT2, Yang JR2, Shirakura M3, Watanabe S3, Odagiri T3, Saito T4,5.

Author information: 1 Division of Transboundary Animal Disease, National Institute of Animal Health, National Agriculture and Food Research Organization (NARO), 3-1-5 Kannondai, Tsukuba, Ibaraki, 305-0856, Japan. 2 Center for Research, Diagnostics and Vaccine Development, Centers for Disease Control, Ministry of Health and Welfare, Taipei, Taiwan. 3 Influenza Virus Research Center, National Institute of Infectious Diseases, 4-7-1 Gakuen, Musashimurayama, Tokyo, 208-0011, Japan. 4 Division of Transboundary Animal Disease, National Institute of Animal Health, National Agriculture and Food Research Organization (NARO), 3-1-5 Kannondai, Tsukuba, Ibaraki, 305-0856, Japan. taksaito@affrc.go.jp. 5 United Graduate School of Veterinary Sciences, Gifu University, 1-1 Yanagido, Gifu, 501-1193, Japan. taksaito@affrc.go.jp.



Human infection by low-pathogenic avian influenza viruses of the H7N9 subtype was first reported in March 2013 in China. Subsequently, these viruses caused five outbreaks through September 2017. In the fifth outbreak, H7N9 virus possessing a multiple basic amino acid insertion in the cleavage site of hemagglutinin emerged and caused 4% of all human infections in that period. To date, H7N9 highly pathogenic avian influenza viruses (HPAIVs) have been isolated from poultry, mostly chickens, as well as the environment. To evaluate the relative infectivity of these viruses in poultry, chickens and ducks were subjected to experimental infection with two H7N9 HPAIVs isolated from humans, namely A/Guangdong/17SF003/2016 and A/Taiwan/1/2017. When chickens were inoculated with the HPAIVs at a dose of 10650% egg infectious dose (EID50), all chickens died within 2-5 days after inoculation, and the viruses replicated in most of the internal organs examined. The 50% lethal doses of A/Guangdong/17SF003/2016 and A/Taiwan/1/2017 in chickens were calculated as 103.3 and 104.7 EID50, respectively. Conversely, none of the ducks inoculated with either virus displayed any clinical signs, and less-efficient virus replication and less shedding were observed in ducks compared to chickens. These findings indicate that chickens, but not ducks, are highly permissive hosts for emerging H7N9 HPAIVs.

PMID: 30539262 DOI: 10.1007/s00705-018-4102-5

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


#Avian #Influenza A (#H7N9) #Model Based on #Poultry Transport #Network in #China (Comput Math Methods Med., abstract)

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

Comput Math Methods Med. 2018 Nov 4;2018:7383170. doi: 10.1155/2018/7383170. eCollection 2018.

Avian Influenza A (H7N9) Model Based on Poultry Transport Network in China.

Zhang J1,2, Jing W1,2, Zhang W3, Jin Z1,2.

Author information: 1 Complex Systems Research Center, Shanxi University, Taiyuan, Shanxi 030006, China. 2 Shanxi Key Laboratory of Mathematical Techniques and Big Data Analysis on Disease Control and Prevention, Shanxi University, Taiyuan, Shanxi 030006, China. 3 Institute of Disease Control and Prevention of PLA, Beijing 100071, China.



In order to analyze the spread of avian influenza A (H7N9), we construct an avian influenza transmission model from poultry (including poultry farm, backyard poultry farm, live-poultry wholesale market, and wet market) to human according to poultry transport network. We obtain the threshold value for the prevalence of avian influenza A (H7N9) and also give the existence and number of the boundary equilibria and endemic equilibria in different conditions. We can see that poultry transport network plays an important role in controlling avian influenza A (H7N9). Finally, numerical simulations are presented to illustrate the effects of poultry in different places on avian influenza. In order to reduce human infections in China, our results suggest that closing the retail live-poultry market or preventing the poultry of backyard poultry farm into the live-poultry market is feasible in a suitable condition.

PMID: 30532797 PMCID: PMC6247641 DOI: 10.1155/2018/7383170 Free full text

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


#Phylogeography of #H5N1 #avian #influenza virus in #Indonesia (Transbound Emerg Dis., abstract)

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

Transbound Emerg Dis. 2018 Oct;65(5):1339-1347. doi: 10.1111/tbed.12883. Epub 2018 Apr 24.

Phylogeography of H5N1 avian influenza virus in Indonesia.

Njoto EN1, Scotch M1,2,3, Bui CM1, Adam DC1, Chughtai AA1, MacIntyre CR1,3,4.

Author information: 1 School of Public Health and Community Medicine, University of New South Wales Sydney, Sydney, NSW, Australia. 2 Center for Environmental Health Engineering, Biodesign Institute, Arizona State University, Tempe, Arizona. 3 College of Health Solutions, Arizona State University, Phoenix, Arizona. 4 College of Public Service and Community Solution, Arizona State University, Phoenix, Arizona.



Highly pathogenic avian influenza (HPAI) viruses of the H5N1 subtype are a major concern to human and animal health in Indonesia. This study aimed to characterize transmission dynamics of H5N1 over time using novel Bayesian phylogeography methods to identify factors which have influenced the spread of H5N1 in Indonesia. We used publicly available hemagglutinin sequence data sampled between 2003 and 2016 to model ancestral state reconstruction of HPAI H5N1 evolution. We found strong support for H5N1 transmission routes between provinces in Java Island and inter-island transmissions, such as between Nusa Tenggara and Kalimantan Islands, not previously described. The spread is consistent with wild bird flyways and poultry trading routes. H5N1 migration was associated with the regions of high chicken densities and low human development indices. These results can be used to inform more targeted planning of H5N1 control and prevention activities in Indonesia.

KEYWORDS: H5N1 Subtype; Indonesia; Influenza A Virus; One Health; Phylogeography

PMID: 29691995 DOI: 10.1111/tbed.12883 [Indexed for MEDLINE]

Keywords: Avian Influenza; H5N1; Indonesia; Wild Birds; Poultry; Human.


Major #contribution of the #RNA-binding domain of #NS1 in the #pathogenicity and replication potential of an #avian #H7N1 #influenza virus in #chickens (Virol J., abstract)

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

Virol J. 2018 Mar 27;15(1):55. doi: 10.1186/s12985-018-0960-4.

Major contribution of the RNA-binding domain of NS1 in the pathogenicity and replication potential of an avian H7N1 influenza virus in chickens.

Trapp S1,2, Soubieux D1,2, Lidove A1,2, Esnault E1,2, Lion A1,2, Guillory V1,2, Wacquiez A1,2, Kut E1,2, Quéré P1,2, Larcher T3,4, Ledevin M3,4, Nadan V5, Camus-Bouclainville C6, Marc D7,8.

Author information: 1 Equipe PIA, UMR1282-ISP Infectiologie et Santé Publique, INRA, 37380, Nouzilly, France. 2 UMR1282 Infectiologie et Santé Publique, Université de Tours, F-37000, Tours, France. 3 INRA UMR 703, APEX, Oniris-La Chantrerie, F-44307, Nantes, France. 4 LUNAM Université, École Nationale Vétérinaire, agro-alimentaire et de l’alimentation Nantes-Atlantique (Oniris), Nantes, France. 5 Centre de Biophysique Moléculaire, CNRS, Orléans, France. 6 IHAP, UMR1225, Université de Toulouse, INRA, ENVT, Toulouse, France. 7 Equipe PIA, UMR1282-ISP Infectiologie et Santé Publique, INRA, 37380, Nouzilly, France. daniel.marc@inra.fr. 8 UMR1282 Infectiologie et Santé Publique, Université de Tours, F-37000, Tours, France. daniel.marc@inra.fr.




Non-structural protein NS1 of influenza A viruses harbours several determinants of pathogenicity and host-range. However it is still unclear to what extent each of its two structured domains (i.e. RNA-binding domain, RBD, and effector domain, ED) contribute to its various activities.


To evaluate the respective contributions of the two domains, we genetically engineered two variants of an H7N1 low pathogenicity avian influenza virus harbouring amino-acid substitutions that impair the functionality of either domain. The RBD- and ED-mutant viruses were compared to their wt- counterpart in vivo and in vitro, notably in chicken infection and avian cell culture models.


The double substitution R38A-K41A in the RBD dramatically reduced the pathogenicity and replication potential of the virus, whereas the substitution A149V that was considered to abrogate the IFN-antagonistic activity of the effector domain entailed much less effects. While all three viruses initiated the viral life cycle in avian cells, replication of the R38A-K41A virus was severely impaired. This defect was associated with a delayed synthesis of nucleoprotein NP and a reduced accumulation of NS1, which was found to reach a concentration of about 30 micromol.L- 1 in wt-infected cells at 8 h post-infection. When overexpressed in avian lung epithelial cells, both the wt-NS1 and 3841AA-NS1, but not the A149V-NS1, reduced the poly(I:C)-induced activation of the IFN-sensitive chicken Mx promoter. Unexpectedly, the R38A-K41A substitution in the recombinant RBD did not alter its in vitro affinity for a model dsRNA. When overexpressed in avian cells, both the wt- and A149V-NS1s, as well as the individually expressed wt-RBD to a lesser extent, enhanced the activity of the reconstituted viral RNA-polymerase in a minireplicon assay.


Collectively, our data emphasized the critical importance and essential role of the RNA-binding domain in essential steps of the virus replication cycle, notably expression and translation of viral mRNAs.

KEYWORDS: Chicken; Influenza A; NS1; Viral replication

PMID: 29587792 PMCID: PMC5870492 DOI: 10.1186/s12985-018-0960-4 [Indexed for MEDLINE]  Free PMC Article

Keywords: Avian Influenza; H7N1; Poultry; Viral pathogenesis.


Closure of live #bird #markets leads to the spread of #H7N9 #influenza in #China (PLoS One, abstract)

[Source: PLoS One, full page: (LINK). Abstract, edited.]


Closure of live bird markets leads to the spread of H7N9 influenza in China

Yin Li, Youming Wang, Chaojian Shen, Jianlong Huang, Jingli Kang, Baoxu Huang, Fusheng Guo, John Edwards

Published: December 12, 2018 / DOI: https://doi.org/10.1371/journal.pone.0208884



Following the emergence of H7N9 influenza in March 2013, local animal and public health authorities in China have been closing live bird markets as a measure to try to control the H7N9 influenza epidemic. The role of live bird market (LBM) closure on the spread of N7N9 influenza following the closure of LBMs during March to May 2013 (the first wave) and October 2013 to March 2014 (the second wave) is described in this paper. Different provinces implemented closure actions at different times, and intensive media reports on H7N9 in different provinces started at different times. Local broiler prices dropped dramatically in places with outbreaks and more live chickens were transported to other LBMs in neighboring areas without human cases from infected areas when live bird markets were being closed. There were six clusters of human infection from March to May 2013 and October 2013 to March 2014 and there may have been intensive poultry transportation among cluster areas. These findings provide evidence that the closure of LBMs in early waves of H7N9 influenza had resulted in expansion of H7N9 infection to uninfected areas. This suggests that provincial authorities in inland provinces should be alert to the risks of sudden changes in movement patterns for live birds after LBM closure or increased publicity about LBM closure.


Citation: Li Y, Wang Y, Shen C, Huang J, Kang J, Huang B, et al. (2018) Closure of live bird markets leads to the spread of H7N9 influenza in China. PLoS ONE 13(12): e0208884. https://doi.org/10.1371/journal.pone.0208884

Editor: Shuo Su, Nanjing Agricultural University, CHINA

Received: February 15, 2018; Accepted: November 27, 2018; Published: December 12, 2018

Copyright: © 2018 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Data Availability: All relevant data are within the paper and its Supporting Information files.

Funding: This study was funded by the National Key R&D Program of China (2017YFC1200500). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist.

Keywords: Avian Influenza; H7N9; Human; Poultry; China; Live birds markets.


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.



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.