#Person-to-Person #Transmission of #Avian #Influenza A (#H7N9) Among #Family Members in Eastern #China, 2016 (Disaster Med Public Health Prep., abstract)

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

Disaster Med Public Health Prep, 1-6 2020 Mar 27 [Online ahead of print]

Person-to-Person Transmission of Avian Influenza A (H7N9) Among Family Members in Eastern China, 2016

Chao Shi # 1, Ping Shi # 1, Xu Yang 1, Jing Bao 2, Yanhua Qian 1, Yuan Shen 1

Affiliations: 1 Departments of Disease Control, Wuxi, Jiangsu Province, China. 2 Laboratory, Wuxi Center for Disease Control and Prevention, Wuxi, Jiangsu Province, China.

Contributed equally.

PMID: 32216856 DOI: 10.1017/dmp.2020.6

 

Abstract

Objective:

Human infections with avian influenza A (H7N9) virus are associated with exposure to poultry and live poultry markets, but the evidence of person-to-person transmission remains limited. This study reports a suspected person-to-person transmission of H7N9 virus, and explores what factors influenced this transmission.

Methods:

We interviewed 2 patients with H7N9 infection and their family members as well as health-care workers. Samples from the patients and environments were tested by real-time reverse transcription-polymerase chain reaction.

Results:

The index patient became ill 5 to 6 days after his last exposure to the poultry bought in the market of Weimiao town. The second patient, the sister of the index patient, who had sustained intensive and unprotected close contact with the index patient, had no exposure to poultry. This study documents that the H7N9 virus was transmitted directly from the index patient to his sister.

Conclusions:

Our findings suggest that person-to-person transmission may be associated with sustained close contact with the patient during his onset of early stage, when the H7N9 viral shedding increases sharply.

Keywords: infection; influenza A (H7N9) virus; person-to-person transmission.

Keywords: Avian Influenza; H7N9; Human; China.

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Higher #virulence of #swine #H1N2 #influenza viruses containing #avian-origin #HA and 2009 #pandemic PA and NP in #pigs and mice (Arch Virol., abstract)

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

Higher virulence of swine H1N2 influenza viruses containing avian-origin HA and 2009 pandemic PA and NP in pigs and mice

Yunyueng Jang, Taehyun Seo & Sang Heui Seo

Archives of Virology (2020)

 

Abstract

Pigs are capable of harbouring influenza A viruses of human and avian origin in their respiratory tracts and thus act as an important intermediary host to generate novel influenza viruses with pandemic potential by genetic reassortment between the two viruses. Here, we show that two distinct H1N2 swine influenza viruses contain avian-like or classical swine-like hemagglutinins with polymerase acidic (PA) and nucleoprotein (NP) genes from 2009 pandemic H1N1 influenza viruses that were found to be circulating in Korean pigs in 2018. Swine H1N2 influenza virus containing an avian-like hemagglutinin gene had enhanced pathogenicity, causing severe interstitial pneumonia in infected pigs and mice. The mortality rate of mice infected with swine H1N2 influenza virus containing an avian-like hemagglutinin gene was higher by 100% when compared to that of mice infected with swine H1N2 influenza virus harbouring classical swine-like hemagglutinin. Further, chemokines attracting inflammatory cells were strongly induced in lung tissues of pigs and mice infected by swine H1N2 influenza virus containing an avian-like hemagglutinin gene. In conclusion, it is necessary for the well-being of humans and pigs to closely monitor swine influenza viruses containing avian-like hemagglutinin with PA and NP genes from 2009 pandemic H1N1 influenza viruses.

Keywords: Influenza A; Avian Influenza; Swine Influenza; H1N1pdm09; H1N2; Reassortant strain; Pigs; Animal models.

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Evaluation of the #immune #response of a #H7N9 candidate #vaccine virus derived from the fifth wave A/Guangdong/17SF003/2016 (Antiviral Res., abstract)

[Source: Antiviral Research, full page: (LINK). Abstract, edited.]

Antiviral Research | Volume 177, May 2020, 104776

Evaluation of the immune response of a H7N9 candidate vaccine virus derived from the fifth wave A/Guangdong/17SF003/2016

Ji Dong a1, Peihai Chen bc1, Yang Wang a1, Yunhua Lv a, Ji Xiao a, Qinming Li a, Zhixia Li c, Beiwu Zhang c, Xuefeng Niu a, Chufang Li a, Weiqi Pan a, Ling Chen a

{a} State Key Laboratory of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China; {b} Institute of Health Sciences and Technology, Anhui University, Hefei, China; {c} State Key Laboratory of Respiratory Disease, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China

Received 28 October 2019, Revised 4 February 2020, Accepted 16 March 2020, Available online 19 March 2020.

DOI: https://doi.org/10.1016/j.antiviral.2020.104776

 

Highlights

  • Systemically evaluated the immune response to H7N9 CVV A/Guangdong/17SF003/2016 (GD/16) in mice and rhesus macaques.
  • GD/16 elicited robust neutralizing and IgG antibodies, but poor hemagglutination inhibition antibody titers.
  • Receptor binding avidity should be considered in interpretation of HI data for evaluation of influenza antigenic variation.

 

Abstract

Highly pathogenic influenza H7N9 viruses that emerged in the fifth wave of H7N9 outbreak pose a risk to human health. The World Health Organization has updated the candidate vaccine viruses for H7N9 viruses recently. In this study, we evaluated the immune response to an updated H7N9 candidate vaccine virus, which derived from the highly pathogenic A/Guangdong/17SF003/2016 (GD/16) in mice and rhesus macaques. GD/16 vaccination elicited robust neutralizing, virus-specific immunoglobulin G antibodies and effective protection, but poor hemagglutination inhibition antibody titers. Furthermore, mouse and rhesus macaque serum raised against the previous H7N9 CVV A/Anhui/1/2013 (AH/13) were tested for its cross-reactivity to GD/16 virus. We found that although AH/13-immune serum has poor hemagglutination inhibition reactivity against GD/16 virus, AH/13 elicit efficient cross-neutralizing antibodies and in vivo protection against GD/16. Further studies showed that the hemagglutinin of GD/16 has strong receptor binding avidity, which might be associated with the decreased hemagglutination inhibition assay sensitivity. This study underscores the point that receptor binding avidity should be taken into account when performing quantitative interpretation of hemagglutination inhibition data. A combination of multiple serological assays is required for accurate vaccine evaluation and antigenic analysis of influenza viruses.

Keywords: H7N9 influenza Virus – Vaccine – Immune response – Cross-reactivity – Haemagglutination inhibition – Receptor binding avidity

Keywords: Avian Influenza; H7N9; Vaccines.

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#Emergence and #Selection of a Highly Pathogenic #Avian #Influenza #H7N3 Virus (J Virol., abstract)

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

J Virol  2020 Jan 22 [Online ahead of print]

Emergence and Selection of a Highly Pathogenic Avian Influenza H7N3 Virus

Nancy Beerens 1, Rene Heutink 2, Frank Harders 2, Alex Bossers 2, Guus Koch 2, Ben Peeters 2

Affiliations: 1 Wageningen Bioveterinary Research, Lelystad, The Netherlands. nancy.beerens@wur.nl. 2 Wageningen Bioveterinary Research, Lelystad, The Netherlands.

PMID: 31969434  DOI: 10.1128/JVI.01818-19

 

Abstract

Low pathogenic avian influenza (LPAI) viruses of subtypes H5 and H7 have the ability to spontaneously mutate to highly pathogenic (HPAI) variants, causing high mortality in poultry. The highly pathogenic phenotype is caused by mutation of the hemagglutinin (HA) cleavage site, but additional mutations may play a role. Evidence from the field for the switch to high pathogenicity remains scarce. This study provides direct evidence for LPAI to HPAI mutation during H7N3 infection of a turkey farm in the Netherlands. No severe clinical symptoms were reported at the farm, but deep-sequencing revealed a minority of HPAI sequences (0.06%) in the virus population isolated from infected turkeys. The HPAI virus contained a 12-nucleotide insertion in the HA cleavage site, that was likely introduced by a single event, as no intermediates with shorter inserts were identified. This suggests non-homologous recombination as the mechanism of insertion. Analysis of different organs of the infected turkeys showed the highest amount of HPAI virus in the lung (4.4%). The HPAI virus was rapidly selected in experimentally infected chickens, after both intravenous and intranasal/intratracheal inoculation with the mixed virus preparation. Full-genome sequencing revealed that both pathotypes contained a deletion in the stalk region of the neuraminidase protein. We identified additional mutations in HA and polymerase basic protein 1 (PB1) in the HPAI virus, which were already present as minority variants in the LPAI virus population. Our findings provide more insight in the molecular changes and mechanisms involved in the emergence and selection of HPAI viruses.

 

IMPORTANCE

Low pathogenic avian influenza (LPAI) viruses circulate in wild birds, and can be transmitted to poultry. LPAI viruses can mutate to become highly pathogenic avian influenza (HPAI) viruses causing severe disease and death in poultry. Little is known about this switch to high pathogenicity. We isolated a LPAI H7N3 virus from an infected turkey farm, and showed that this contains small amounts of HPAI virus. The HPAI virus rapidly outcompeted the LPAI virus in chickens that were experimentally infected with this mixture of viruses. We analysed the genome sequences of the LPAI and HPAI viruses, and identified several changes that may be important for a virus to become highly pathogenic. This knowledge may be used for timely identification of LPAI viruses that pose a risk of becoming highly pathogenic in the field.

Copyright © 2020 American Society for Microbiology.

Keywords: Avian Influenza; H7N3; Poultry; Netherlands.

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Specificity, #Kinetics and Longevity of #Antibody #Responses to #Avian #Influenza A(#H7N9) Virus #Infection in #Humans (J Infect., abstract)

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

J Infect. 2020 Jan 16. pii: S0163-4453(20)30025-6. doi: 10.1016/j.jinf.2019.11.024. [Epub ahead of print]

Specificity, Kinetics and Longevity of Antibody Responses to Avian Influenza A(H7N9) Virus Infection in Humans.

Chen J1, Zhu H2, Horby PW3, Wang Q1, Zhou J1, Jiang H4, Liu L5, Zhang T6, Zhang Y7, Chen X1, Deng X1, Nikolay B8, Wang W1, Cauchemez S8, Guan Y2, Uyeki TM9, Yu H10.

Author information: 1 School of Public Health, Fudan University, Key Laboratory of Public Health Safety, Ministry of Education, Shanghai, 200032, China. 2 Joint Institute of Virology (STU-HKU), Shantou University, Shantou, 515041, China; State Key Laboratory of Emerging Infectious Diseases, School of Public Health, The University of Hong Kong, Hong Kong SAR, China. 3 Centre for Tropical Medicine and Global Health, University of Oxford, Oxford, UK. 4 Beijing Chest Hospital, Capital Medical University, Beijing, 101149, China; Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing, 101149, China. 5 Joint Institute of Virology (STU-HKU), Shantou University, Shantou, 515041, China. 6 Jiangxi Provincial Center for Disease Control and Prevention, Nanchang, 330000, China. 7 Savaid Medical School, University of Chinese Academy of Sciences, Beijing, 100049, China. 8 Mathematical Modelling of Infectious Diseases Unit, Institut Pasteur, UMR2000, CNRS, 75015 Paris, France. 9 Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, USA. 10 School of Public Health, Fudan University, Key Laboratory of Public Health Safety, Ministry of Education, Shanghai, 200032, China. Electronic address: yhj@fudan.edu.cn.

 

Abstract

OBJECTIVES:

The long-term dynamics of antibody responses in patients with influenza A(H7N9) virus infection are not well understood.

METHODS:

We conducted a longitudinal serological follow-up study in patients who were hospitalized with A(H7N9) virus infection, during 2013-2018. A(H7N9) virus-specific antibody responses were assessed by hemagglutination inhibition (HAI) and neutralization (NT) assays. A random intercept model was used to fit a curve to HAI antibody responses over time. HAI antibody responses were compared by clinical severity.

RESULTS:

Of 67 patients with A(H7N9) virus infection, HAI antibody titers reached 40 on average 11 days after illness onset and peaked at a titer of 290 after three months, and average titers of ≥80 and ≥40 were present until 11 months and 22 months respectively. HAI antibody responses were significantly higher in patients who experienced severe disease, including respiratory failure and acute respiratory distress syndrome, compared with patients who experienced less severe illness.

CONCLUSIONS:

Patients with A(H7N9) virus infection who survived severe disease mounted higher antibody responses that persisted for longer periods compared with those that experienced moderate disease. Studies of convalescent plasma treatment for A(H7N9) patients should consider collection of donor plasma from survivors of severe disease between 1-11 months after illness onset.

Copyright © 2020 Elsevier Ltd. All rights reserved.

KEYWORDS: Antibody response; Clinical severity; Follow-up; Influenza A(H7N9)

PMID: 31954742 DOI: 10.1016/j.jinf.2019.11.024

Keywords: Avian Influenza; H7N9; Serotherapy; Human.

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#H7N9 #Influenza Virus Containing a #Polybasic HA Cleavage Site Requires Minimal Host #Adaptation to Obtain a Highly Pathogenic Disease Phenotype in Mice (Viruses, abstract)

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

Viruses. 2020 Jan 5;12(1). pii: E65. doi: 10.3390/v12010065.

H7N9 Influenza Virus Containing a Polybasic HA Cleavage Site Requires Minimal Host Adaptation to Obtain a Highly Pathogenic Disease Phenotype in Mice.

Chan M1, Leung A1, Hisanaga T2, Pickering B2,3, Griffin BD1,3, Vendramelli R1, Tailor N1, Wong G4,5, Bi Y6, Babiuk S2, Berhane Y2, Kobasa D1,3.

Author information: 1 Special Pathogens Program, National Microbiology Laboratory, Public Health Agency of Canada, 1015 Arlington Street, Winnipeg, MB R3E 3R2, Canada. 2 National Centre for Foreign Animal Disease, Canadian Food Inspection Agency, Winnipeg, MB R3E 3M4, Canada. 3 Department of Medical Microbiology and Infectious Diseases, University of Manitoba, 745 Bannatyne Avenue, Winnipeg, MB R3E 0J9, Canada. 4 Institut Pasteur of Shanghai, Chinese Academy of Sciences, Life Science Research Building 320 Yueyang Road, Xuhui District, Shanghai 200031, China. 5 Département de microbiologie-infectiologie et d’immunologie, Université Laval, 1050 avenue de la Médecine, QC G1V 0A6, Canada. 6 CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Center for Influenza Research and Early-warning (CASCIRE), Chinese Academy of Sciences, Beijing 100101, China.

 

Abstract

Low pathogenic avian influenza (LPAI) H7N9 viruses have recently evolved to gain a polybasic cleavage site in the hemagglutinin (HA) protein, resulting in variants with increased lethality in poultry that meet the criteria for highly pathogenic avian influenza (HPAI) viruses. Both LPAI and HPAI variants can cause severe disease in humans (case fatality rate of ~40%). Here, we investigated the virulence of HPAI H7N9 viruses containing a polybasic HA cleavage site (H7N9-PBC) in mice. Inoculation of mice with H7N9-PBC did not result in observable disease; however, mice inoculated with a mouse-adapted version of this virus, generated by a single passage in mice, caused uniformly lethal disease. In addition to the PBC site, we identified three other mutations that are important for host-adaptation and virulence in mice: HA (A452T), PA (D347G), and PB2 (M483K). Using reverse genetics, we confirmed that the HA mutation was the most critical for increased virulence in mice. Our study identifies additional disease determinants in a mammalian model for HPAI H7N9 virus. Furthermore, the ease displayed by the virus to adapt to a new host highlights the potential for H7N9-PBC viruses to rapidly acquire mutations that may enhance their risk to humans or other animal species.

KEYWORDS: H7N9; HPAI; influenza virus; mammalian adaptation; mice; polybasic HA

PMID: 31948040 DOI: 10.3390/v12010065

Keywords: Avian Influenza; H7N9; Viral pathogenesis; Animal models.

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#Molecular, #antigenic, and #pathogenic characterization of #H5N8 highly pathogenic #avian #influenza viruses isolated in the #DRC in 2017 (Arch Virol., abstract)

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

Arch Virol. 2020 Jan;165(1):87-96. doi: 10.1007/s00705-019-04456-x. Epub 2019 Nov 9.

Molecular, antigenic, and pathogenic characterization of H5N8 highly pathogenic avian influenza viruses isolated in the Democratic Republic of Congo in 2017.

Twabela AT1,2, Okamatsu M1, Tshilenge GM2, Mpiana S2, Masumu J2, Nguyen LT1, Matsuno K1,3, Monne I4, Zecchin B4, Sakoda Y5,6.

Author information: 1 Laboratory of Microbiology, Department of Disease Control, Faculty of Veterinary Medicine, Hokkaido University, North 18, West 9, Kita-ku, Sapporo, Hokkaido, 060-0818, Japan. 2 Central Veterinary Laboratory of Kinshasa, Kinshasa I, Gombe, Democratic Republic of Congo. 3 Global Station for Zoonosis Control, Global Institution for Collaborative Research and Education (GI-CoRE), Hokkaido University, Sapporo, Hokkaido, Japan. 4 Istituto Zooprofilattico Sperimentale Delle Venezie, Legnaro, PD, Italy. 5 Laboratory of Microbiology, Department of Disease Control, Faculty of Veterinary Medicine, Hokkaido University, North 18, West 9, Kita-ku, Sapporo, Hokkaido, 060-0818, Japan. sakoda@vetmed.hokudai.ac.jp. 6 Global Station for Zoonosis Control, Global Institution for Collaborative Research and Education (GI-CoRE), Hokkaido University, Sapporo, Hokkaido, Japan. sakoda@vetmed.hokudai.ac.jp.

 

Abstract

In May 2017, high mortality of chickens and Muscovy ducks due to the H5N8 highly pathogenic avian influenza virus (HPAIV) was reported in the Democratic Republic of Congo (DR Congo). In this study, we assessed the molecular, antigenic, and pathogenic features in poultry of the H5N8 HPAIV from the 2017 Congolese outbreaks. Phylogenetic analysis of the eight viral gene segments revealed that all 12 DR Congo isolates clustered in clade 2.3.4.4B together with other H5N8 HPAIVs isolated in Africa and Eurasia, suggesting a possible common origin of these viruses. Antigenically, a slight difference was observed between the Congolese isolates and a representative virus from group C in the same clade. After intranasal inoculation with a representative DR Congo virus, high pathogenicity was observed in chickens and Muscovy ducks but not in Pekin ducks. Viral replication was higher in chickens than in Muscovy duck and Pekin duck organs; however, neurotropism was pronounced in Muscovy ducks. Our data confirmed the high pathogenicity of the DR Congo virus in chickens and Muscovy ducks, as observed in the field. National awareness and strengthening surveillance in the region are needed to better control HPAIVs.

PMID: 31707455 DOI: 10.1007/s00705-019-04456-x [Indexed for MEDLINE]

Keywords: Avian Influenza; H5N8; Poultry; DRC.

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