#EIDs: Focus on #infection #control #issues for novel #coronaviruses (#SARS-CoV & #MERS-CoV), #VHF (#Lassa and #Ebola), and HPAI viruses, #H5N1 & #H7N9 (SD, abstract)

[Source: Science Direct, full page: (LINK). Abstract, edited.]

American Journal of Infection Control / Volume 44, Issue 5, Supplement, 2 May 2016, Pages e91–e100  / Disinfection, Sterilization and Antisepsis: Principles, Practices, Current Issues, New Research and New Technologies / Major article

Emerging infectious diseases: Focus on infection control issues for novel coronaviruses (Severe Acute Respiratory Syndrome-CoV and Middle East Respiratory Syndrome-CoV), hemorrhagic fever viruses (Lassa and Ebola), and highly pathogenic avian influenza viruses, A(H5N1) and A(H7N9)

David J. Weber, MD, MPHa, b,  William A. Rutala, PhD, MPHa, b, William A. Fischer, MDc, Hajime Kanamori, MD, PhD, MPHa, b, Emily E. Sickbert-Bennett, PhD, MSa, b

a Department of Hospital Epidemiology, University of North Carolina Health Care, Chapel Hill, NC; b Division of Infectious Diseases, University of North Carolina School of Medicine, Chapel Hill, NC; c Division of Pulmonary and Critical Care Medicine, University of North Carolina School of Medicine, Chapel Hill, NC

Available online 28 April 2016 / doi:10.1016/j.ajic.2015.11.018

 

Abstract

Over the past several decades, we have witnessed the emergence of many new infectious agents, some of which are major public threats. New and emerging infectious diseases which are both transmissible from patient-to-patient and virulent with a high mortality include novel coronaviruses (SARS-CoV, MERS-CV), hemorrhagic fever viruses (Lassa, Ebola), and highly pathogenic avian influenza A viruses, A(H5N1) and A(H7N9). All healthcare facilities need to have policies and plans in place for early identification of patients with a highly communicable diseases which are highly virulent, ability to immediately isolate such patients, and provide proper management (e.g., training and availability of personal protective equipment) to prevent transmission to healthcare personnel, other patients and visitors to the healthcare facility.

Key Words: Emerging infectious diseases; health care–associated infections; infection control; occupational health; severe acute respiratory disease; Middle East respiratory syndrome; Lassa fever; Ebola viral disease; novel influenza viruses

Funding/support: Supported by the University of North Carolina at Chapel Hill (U54CK000164).

Publication of this article was supported by an educational grant from Clorox Healthcare, Sealed Air, and Tru-D. Content of this article was initiated and written by the authors with no input or financial support to the authors from Clorox Healthcare, Sealed Air, or Tru-D.

Conflicts of Interest: None to report.

Address correspondence to David J. Weber, MD, MPH, 2163 Bioinformatics, CB #7030, Chapel Hill, NC 27599-7030. (D.J. Weber).

© 2015 Association for Professionals in Infection Control and Epidemiology, Inc. Published by Elsevier Inc. All rights reserved.

Keywords: Research; Abstracts; Lassa Fever; Ebola; H7N9; H5N1; Avian Influenza; MERS-CoV; SARS-CoV.

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#Lack of #chicken #adaptation of newly emergent #Eurasian #H5N8 and reassortant #H5N2 HPAI #viruses in the #US is consistent with restricted #poultry #outbreaks … (Virology, abstract)

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

Virology. 2016 Apr 22;494:190-197. doi: 10.1016/j.virol.2016.04.019. [Epub ahead of print]

Lack of chicken adaptation of newly emergent Eurasian H5N8 and reassortant H5N2 high pathogenicity avian influenza viruses in the U.S. is consistent with restricted poultry outbreaks in the Pacific flyway during 2014-2015.

Bertran K1, Swayne DE2, Pantin-Jackwood MJ3, Kapczynski DR4, Spackman E5, Suarez DL6.

Author information: 1Exotic and Emerging Avian Viral Diseases Research Unit, Southeast Poultry Research Laboratory, U.S. National Poultry Research Center, Agricultural Research Service, U.S. Department of Agriculture, 934 College Station Rd, 30605 Athens, GA, USA. Electronic address: kateri.bertran@ars.usda.gov. 2Exotic and Emerging Avian Viral Diseases Research Unit, Southeast Poultry Research Laboratory, U.S. National Poultry Research Center, Agricultural Research Service, U.S. Department of Agriculture, 934 College Station Rd, 30605 Athens, GA, USA. Electronic address: david.swayne@ars.usda.gov. 3Exotic and Emerging Avian Viral Diseases Research Unit, Southeast Poultry Research Laboratory, U.S. National Poultry Research Center, Agricultural Research Service, U.S. Department of Agriculture, 934 College Station Rd, 30605 Athens, GA, USA. Electronic address: mary.pantin-jackwood@ars.usda.gov. 4Exotic and Emerging Avian Viral Diseases Research Unit, Southeast Poultry Research Laboratory, U.S. National Poultry Research Center, Agricultural Research Service, U.S. Department of Agriculture, 934 College Station Rd, 30605 Athens, GA, USA. Electronic address: darrell.kapczynski@ars.usda.gov. 5Exotic and Emerging Avian Viral Diseases Research Unit, Southeast Poultry Research Laboratory, U.S. National Poultry Research Center, Agricultural Research Service, U.S. Department of Agriculture, 934 College Station Rd, 30605 Athens, GA, USA. Electronic address: erica.spackman@ars.usda.gov. 6Exotic and Emerging Avian Viral Diseases Research Unit, Southeast Poultry Research Laboratory, U.S. National Poultry Research Center, Agricultural Research Service, U.S. Department of Agriculture, 934 College Station Rd, 30605 Athens, GA, USA. Electronic address: david.suarez@ars.usda.gov.

 

Abstract

In 2014-2015, the U.S. experienced an unprecedented outbreak of Eurasian clade 2.3.4.4 H5 highly pathogenic avian influenza (HPAI) virus, initially affecting mainly wild birds and few backyard and commercial poultry premises. To better model the outbreak, the pathogenesis and transmission dynamics of representative Eurasian H5N8 and reassortant H5N2 clade 2.3.4.4 HPAI viruses detected early in the North American outbreak were investigated in chickens. High mean chicken infectious doses and lack of seroconversion in survivors indicated the viruses were poorly chicken adapted. Pathobiological features were consistent with HPAI virus infection, although the delayed appearance of lesions, longer mean death times, and reduced replication in endothelial cells differed from features of most other Eurasian H5N1 HPAI viruses. Although these initial U.S. H5 HPAI viruses had reduced adaptation and transmissibility in chickens, multi-generational passage in poultry could generate poultry adapted viruses with higher infectivity and transmissibility.

Copyright © 2016. Published by Elsevier Inc.

KEYWORDS: Avian influenza; Clade 2.3.4.4; Highly pathogenic avian influenza; Infectivity; Pathobiology; Poultry; Transmission; Wild waterfowl

PMID: 27110710 [PubMed – as supplied by publisher]

Keywords: Research; Abstracts; H5N2; H5N8; Reassortant Strains; Avian Influenza; Poultry; USA.

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The #replication of #Bangladeshi #H9N2 #avian #influenza #viruses carrying genes from #H7N3 in #mammals (Emerg Microbes Infect., abstract)

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

Emerg Microbes Infect. 2016 Apr 20;5:e35. doi: 10.1038/emi.2016.29.

The replication of Bangladeshi H9N2 avian influenza viruses carrying genes from H7N3 in mammals.

Shanmuganatham KK1, Jones JC1, Marathe BM1, Feeroz MM2, Jones-Engel L3, Walker D1, Turner J1, Rabiul Alam SM2, Kamrul Hasan M2, Akhtar S2, Seiler P1, McKenzie P1, Krauss S1, Webby RJ1, Webster RG1.

Author information: 1Department of Infectious Diseases, St Jude Children’s Research Hospital, Memphis, TN 38105, USA. 2Department of Zoology, Jahangirnagar University, Dhaka 1342, Bangladesh. 3National Primate Research Center University of Washington, Seattle, WA 98195-5502, USA.

 

Abstract

H9N2 avian influenza viruses are continuously monitored by the World Health Organization because they are endemic; they continually reassort with H5N1, H7N9 and H10N8 viruses; and they periodically cause human infections. We characterized H9N2 influenza viruses carrying internal genes from highly pathogenic H7N3 viruses, which were isolated from chickens or quail from live-bird markets in Bangladesh between 2010 and 2013. All of the H9N2 viruses used in this study carried mammalian host-specific mutations. We studied their replication kinetics in normal human bronchoepithelial cells and swine tracheal and lung explants, which exhibit many features of the mammalian airway epithelium and serve as a mammalian host model. All H9N2 viruses replicated to moderate-to-high titers in the normal human bronchoepithelial cells and swine lung explants, but replication was limited in the swine tracheal explants. In Balb/c mice, the H9N2 viruses were nonlethal, replicated to moderately high titers and the infection was confined to the lungs. In the ferret model of human influenza infection and transmission, H9N2 viruses possessing the Q226L substitution in hemagglutinin replicated well without clinical signs and spread via direct contact but not by aerosol. None of the H9N2 viruses tested were resistant to the neuraminidase inhibitors. Our study shows that the Bangladeshi H9N2 viruses have the potential to infect humans and highlights the importance of monitoring and characterizing this influenza subtype to better understand the potential risk these viruses pose to humans.

PMID: 27094903 [PubMed – in process]

Keywords: Research; Abstracts; Avian Influenza; H7N3; H9N2; Reassortant Strain.

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Novel #Polymerase #Gene #Mutations for #Human #Adaptation in #Clinical Isolates of #Avian #H5N1 #Influenza #Viruses (PLoS Pathog., abstract)

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

Open Access / Peer-reviewed / Research Article

Novel Polymerase Gene Mutations for Human Adaptation in Clinical Isolates of Avian H5N1 Influenza Viruses

Yasuha Arai, Norihito Kawashita, Tomo Daidoji, Madiha S. Ibrahim, Emad M. El-Gendy, Tatsuya Takagi, Kazuo Takahashi, Yasuo Suzuki, Kazuyoshi Ikuta, Takaaki Nakaya, Tatsuo Shioda, Yohei Watanabe

PLOS / Published: April 20, 2016 / http://dx.doi.org/10.1371/journal.ppat.1005583

 

Abstract

A major determinant in the change of the avian influenza virus host range to humans is the E627K substitution in the PB2 polymerase protein. However, the polymerase activity of avian influenza viruses with a single PB2-E627K mutation is still lower than that of seasonal human influenza viruses, implying that avian viruses require polymerase mutations in addition to PB2-627K for human adaptation. Here, we used a database search of H5N1 clade 2.2.1 virus sequences with the PB2-627K mutation to identify other polymerase adaptation mutations that have been selected in infected patients. Several of the mutations identified acted cooperatively with PB2-627K to increase viral growth in human airway epithelial cells and mouse lungs. These mutations were in multiple domains of the polymerase complex other than the PB2-627 domain, highlighting a complicated avian-to-human adaptation pathway of avian influenza viruses. Thus, H5N1 viruses could rapidly acquire multiple polymerase mutations that function cooperatively with PB2-627K in infected patients for optimal human adaptation.

Author Summary

Avian influenza (AI) virus H5N1 subtype strains have been sporadically transmitted to humans with high mortality (>60%), presenting a serious global health threat. In particular, 63% of recent human H5N1 infection cases worldwide have been reported in Egypt, which is now regarded as a hot spot for H5N1 virus evolution. H5N1 clade 2.2.1 viruses are unique to Egypt and probably have the greatest evolutionary potential for adaptation from avian to human hosts. Here, using a comprehensive database approach, we identified various novel polymerase mutations in clade 2.2.1 virus strains, isolated from patients, that enabled enhanced viral replication in both human airway epithelial cells and mouse lungs. Interestingly, the mutations identified acted cooperatively with the PB2-E627K mutation, the most well-known human adaptation mutation, to produce a further increase in viral replication in human hosts. These results provide the first broad-spectrum data on the polymerase characteristics of AI viruses that have been selected in infected patients, and also give new insight into the human adaptation mechanisms of AI viruses.

______

Citation: Arai Y, Kawashita N, Daidoji T, Ibrahim MS, El-Gendy EM, Takagi T, et al. (2016) Novel Polymerase Gene Mutations for Human Adaptation in Clinical Isolates of Avian H5N1 Influenza Viruses. PLoS Pathog 12(4): e1005583. doi:10.1371/journal.ppat.1005583

Editor: Kanta Subbarao, National Institutes of Health, UNITED STATES

Received: November 2, 2015; Accepted: March 28, 2016; Published: April 20, 2016

Copyright: © 2016 Arai 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 work was supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan (KAKENHI Grant Numbers 15K08497 and 15H05295; https://www.jsps.go.jp/english/index.html). 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: Research; Abstracts; H5N1; Avian Influenza; Human.

——

#Hemagglutinin #aminoacids related to #receptor specificity could affect the #protection efficacy of #H5N1 and #H7N9 avian #influenza virus #vaccines in mice (Vaccine, abstract)

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

Vaccine. 2016 Apr 12. pii: S0264-410X(16)30004-4. doi: 10.1016/j.vaccine.2016.03.031. [Epub ahead of print]

Hemagglutinin amino acids related to receptor specificity could affect the protection efficacy of H5N1 and H7N9 avian influenza virus vaccines in mice.

Xu L1, Bao L1, Lau SY2, Wu WL2, Yuan J1, Gu S1, Li F1, Lv Q1, Xu Y1, Pushko P3, Chen H2, Qin C4.

Author information: 1Institute of Laboratory Animal Sciences, Chinese Academy of Medical Sciences (CAMS) and Comparative Medicine Center, Peking Union Medical College (PUMC); Key Laboratory of Human Disease Comparative Medicine, Ministry of Health, Beijing, China. 2State Key Laboratory for Emerging Infectious Diseases, Department of Microbiology and the Research Centre of Infection and Immunology, The University of Hong Kong, 21 Sassoon Road, Pokfulam, Hong Kong, SAR, China. 3Medigen, 8420 Gas House Pike Suite S, Frederick, MD 21701, USA. 4Institute of Laboratory Animal Sciences, Chinese Academy of Medical Sciences (CAMS) and Comparative Medicine Center, Peking Union Medical College (PUMC); Key Laboratory of Human Disease Comparative Medicine, Ministry of Health, Beijing, China. Electronic address: qinchuan@cnilas.org.

 

Abstract

The continuous and sporadic human transmission of highly pathogenic avian H5N1 and H7N9 influenza viruses illustrates the urgent need for efficacious vaccines. However, all tested vaccines for the H5N1 and H7N9 viruses appear to be poorly immunogenic in mammals. In this study, a series of vaccines was produced using reverse genetic techniques that possess HA and NA genes from the H5N1 virus in the genetic background of the high-yield strain A/PR/8/34 (H1N1). Meanwhile, a group of H7N9 VLP vaccines that contain HA from H7N9 and NA and M1 from A/PR/8/34 (H1N1) was also produced. The HA amino acids of both the H5N1 and H7N9 vaccines differed at residues 226 and 228, both of which are critical for receptor specificity for an avian or mammalian host. Mice received two doses (3μg of HA each) of each vaccine and were challenged with lethal doses of wild type H5N1 or H7N9 viruses. The results showed that a recombinant H5N1 vaccine in which the HA amino acid G228 (avian specificity) was converted to S228 (mammalian specificity) resulted in higher HI titers, a lower viral titer in the lungs, and 100% protection in mice. However, a H7N9 VLP vaccine that contains L226 (mammalian specificity) and G228 (avian specificity) in HA showed better immunogenicity and protection efficacy in mice than VLP containing HA with either L226+S228 or Q226+S228. This observation indicated that specific HA residues could enhance a vaccine’s protection efficacy and HA glycoproteins with both avian-type and human-type receptor specificities may produce better pandemic influenza vaccines for humans.

Copyright © 2016 Elsevier Ltd. All rights reserved.

KEYWORDS: Animal model; Influenza; Receptor specificity; Reverse genetics; Vaccine

PMID: 27083426 [PubMed – as supplied by publisher]

Keywords: Research; Abstracts; H5N1; H7N9; Avian Influenza; Vaccines.

——

#Living with #avian #FLU⬝Persistence of the #H5N1 highly pathogenic avian influenza virus in #Egypt (Vet Microbiol., abstract)

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

Vet Microbiol. 2016 May 1;187:82-92. doi: 10.1016/j.vetmic.2016.03.009. Epub 2016 Mar 19.

Living with avian FLU⬝Persistence of the H5N1 highly pathogenic avian influenza virus in Egypt.

Njabo KY1, Zanontian L2, Sheta BN3, Samy A4, Galal S4, Schoenberg FP2, Smith TB5.

Author information: 1Center for Tropical Research, Institute of the Environment and Sustainability, University of California, Los Angeles, United States. Electronic address: kynjabo@ucla.edu. 2Department of Statistics, 8105H Math Sciences Bldg., University of California, Los Angeles, United States. 3Zoology Department, Faculty of Science, Damietta University, P.O. Box 819, 34517 New Damietta, Damietta, Egypt. 4National Laboratory for Veterinary Quality Control on Poultry Production (NLQP), Animal Health Research Institute, P.O. Box 264, Nadi El Said Street, Dokki, Giza, Egypt. 5Center for Tropical Research, Institute of the Environment and Sustainability, University of California, Los Angeles, United States; Department of Ecology and Evolutionary Biology, University of California, Los Angeles, United States.

 

Abstract

H5N1 highly pathogenic avian influenza virus (HPAIV) continues to cause mortality in poultry and threaten human health at a panzootic scale in Egypt since it was reported in 2006. While the early focus has been in Asia, recent evidence suggests that Egypt is an emerging epicenter for the disease. Despite control measures, epizootic transmission of the disease continues. Here, we investigate the persistence of HPAIV across wild passerine birds and domestic poultry between 2009 and 2012 and the potential risk for continuous viral transmission in Egypt. We use a new weighted cross J-function to investigate the degree and spatial temporal nature of the clustering between sightings of infected birds of different types, and the risk of infection associated with direct contact with infected birds. While we found no infection in wild birds, outbreaks occurred year round between 2009 and 2012, with a positive interaction between chickens and ducks. The disease was more present in the years 2010 and 2011 coinciding with the political unrest in the country. Egypt thus continues to experience endemic outbreaks of avian influenza HPAIV in poultry and an increased potential risk of infection to other species including humans. With the current trends, the elimination of the HPAIV infection is highly unlikely without a complete revamp of current policies. The application of spatial statistics techniques to these types of data may help us to understand the characteristics of the disease and may subsequently allow practitioners to explore possible preventive solutions.

Copyright © 2016 Elsevier B.V. All rights reserved.

KEYWORDS: Birds; Cross J-function; Egypt; Influenza A virus; RT-PCR

PMID: 27066713 [PubMed – in process]

Keywords: Research; Abstracts; Avian Influenza; H5N1; Egypt.

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#Adaptive #aminoacid #substitutions enhance the #virulence of a novel #human #H7N9 #influenza #virus in mice (Vet Microbiol., abstract)

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

Vet Microbiol. 2016 May 1;187:8-14. doi: 10.1016/j.vetmic.2016.02.027. Epub 2016 Mar 3.

Adaptive amino acid substitutions enhance the virulence of a novel human H7N9 influenza virus in mice.

Zhao Y1, Yu Z2, Liu L1, Wang T1, Sun W1, Wang C1, Xia Z1, Gao Y3, Zhou B1, Qian J4, Xia X5.

Author information: 1Key Laboratory of Jilin Province for Zoonosis Prevention and Control, Military Veterinary Research Institute, Academy of Military Medical Sciences, Changchun 130122, People’s Republic of China. 2Key Laboratory of Jilin Province for Zoonosis Prevention and Control, Military Veterinary Research Institute, Academy of Military Medical Sciences, Changchun 130122, People’s Republic of China; Institute of Laboratory Animal Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100021, People’s Republic of China. 3Key Laboratory of Jilin Province for Zoonosis Prevention and Control, Military Veterinary Research Institute, Academy of Military Medical Sciences, Changchun 130122, People’s Republic of China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou 225009, People’s Republic of China. 4Key Laboratory of Jilin Province for Zoonosis Prevention and Control, Military Veterinary Research Institute, Academy of Military Medical Sciences, Changchun 130122, People’s Republic of China. Electronic address: qianj1970@126.com. 5Key Laboratory of Jilin Province for Zoonosis Prevention and Control, Military Veterinary Research Institute, Academy of Military Medical Sciences, Changchun 130122, People’s Republic of China; Institute of Laboratory Animal Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100021, People’s Republic of China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou 225009, People’s Republic of China; Beijing Institute of Biotechnology, Beijing 100071, People’s Republic of China. Electronic address: xiaxzh@cae.cn.

 

Abstract

To identify molecular features that confer enhanced H7N9 virulence in mammals, we independently generated three mouse-adapted variants of A/Shanghai/2/2013 (H7N9) by serial passage in mice. The mouse lethal doses (MLD50) of the mouse-adapted variants were reduced >1000-100000-fold when compared to the parental virus. Adapted variants displayed enhanced replication kinetics in vivo, and were capable of replicating in multiple organs. Analysis of adapted viral genomes revealed a total of 14 amino acid changes among the three variant viruses in the PA (T97I, K328R, P332T, and Q556R), HA (H3 numbering; A107T, R220I, L226Q, and R354K), NP (A284T and M352I), NA (M26I, N142S, and G389D), and M1 (M128R) proteins. Notably, many of these adaptive amino acid changes have been identified in naturally occurring H7 isolates. Our results identify amino acid substitutions that collectively enhance the ability of a human H7N9 virus to replicate and cause severe disease in mice.

Copyright © 2016 Elsevier B.V. All rights reserved.

KEYWORDS: Amino acid substitutions; H7N9 influenza virus; Mouse model; Virulence

PMID: 27066703 [PubMed – in process]

Keywords: Research; Abstracts; H7N9; Avian Influenza.

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