Special Issue "Evolution and Pathogenesis of Avian and Animal Influenza Viruses"

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Animal Viruses".

Deadline for manuscript submissions: 31 December 2020.

Special Issue Editors

Dr. El-Sayed M Abdelwhab
E-Mail Website
Guest Editor
Laboratory for Avian Influenza VirusInstitute of Molecular Virology and Cell BiologyFederal Research Institute for Animal Health, Friedrich-Loeffler-InstitutSüdufer 10, 17493 Greifswald - Insel Riems, Germany
Dr. Angele Breithaupt
E-Mail Website
Guest Editor
Laboratory for Pathology II Department of Experimental Animal Facilities and Biorisk Management Federal Research Institute for Animal Health, Friedrich-Loeffler-Institut Südufer 10, 17493 Greifswald - Insel Riems, Germany

Special Issue Information

Dear Colleagues,

Emerging and re-emerging influenza viruses pose a continuous threat to animal and human health. We are facing a highly mutable virus seeking adaptation on different hosts and in harsh environmental conditions. Despite extensive research, particularly to detect, identify, and characterize (novel) influenza viruses in different animal species, vigilance is warranted to monitor changes in virus–host ecology that enable efficient adaptation, high virulence, and interspecies transmission. In this Special Issue, we welcome articles, short communications, case reports, reviews, and commentaries on the evolution and pathogenesis of influenza viruses in birds and mammals. The scope of this SI is to gather papers on, but not limited to, genetic and evolutionary analysis, genetic determinants for virulence and adaptation in birds and mammals, assessment of pathogenicity and transmission, virus–host–ecology interaction, macro- and microscopic alterations, tropism to different organs/cells, epidemiological investigation, and development of new laboratory tools for diagnosis and characterization of influenza viruses.

Dr. El-Sayed M Abdelwhab
Dr. Angele Breithaupt
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Avian influenza
  • pathogenesis
  • virus evolution
  • zoonotic diseases
  • pandemic
  • tropism
  • animals
  • birds
  • reservoir
  • virulence determinants

Published Papers (3 papers)

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Research

Open AccessArticle
Detection of a Reassortant H9N2 Avian Influenza Virus with Intercontinental Gene Segments in a Resident Australian Chestnut Teal
Viruses 2020, 12(1), 88; https://doi.org/10.3390/v12010088 - 13 Jan 2020
Abstract
The present study reports the genetic characterization of a low-pathogenicity H9N2 avian influenza virus, initially from a pool and subsequently from individual faecal samples collected from Chestnut teals (Anas castanea) in southeastern Australia. Phylogenetic analyses of six full gene segments and [...] Read more.
The present study reports the genetic characterization of a low-pathogenicity H9N2 avian influenza virus, initially from a pool and subsequently from individual faecal samples collected from Chestnut teals (Anas castanea) in southeastern Australia. Phylogenetic analyses of six full gene segments and two partial gene segments obtained from next-generation sequencing showed that this avian influenza virus, A/Chestnut teal/Australia/CT08.18/12952/2018 (H9N2), was a typical, low-pathogenicity, Eurasian aquatic bird lineage H9N2 virus, albeit containing the North American lineage nucleoprotein (NP) gene segment detected previously in Australian wild birds. This is the first report of a H9N2 avian influenza virus in resident wild birds in Australia, and although not in itself a cause of concern, is a clear indication of spillover and likely reassortment of influenza viruses between migratory and resident birds, and an indication that any lineage could potentially be introduced in this way. Full article
(This article belongs to the Special Issue Evolution and Pathogenesis of Avian and Animal Influenza Viruses)
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Open AccessArticle
Infection of Human Tracheal Epithelial Cells by H5 Avian Influenza Virus Is Regulated by the Acid Stability of Hemagglutinin and the pH of Target Cell Endosomes
Viruses 2020, 12(1), 82; https://doi.org/10.3390/v12010082 - 09 Jan 2020
Abstract
Despite the possible relationships between tracheal infection and concomitant infection of the terminal part of the lower respiratory tract (bronchioles/alveoli), the behavior of avian influenza viruses (AIVs), such as H5N1, in the conducting airways is unclear. To examine the tropism of AIVs for [...] Read more.
Despite the possible relationships between tracheal infection and concomitant infection of the terminal part of the lower respiratory tract (bronchioles/alveoli), the behavior of avian influenza viruses (AIVs), such as H5N1, in the conducting airways is unclear. To examine the tropism of AIVs for cells lining the conducting airways of humans, we established human tracheal epithelial cell clones (HTEpC-Ts) and examined their susceptibility to infection by AIVs. The HTEpC-Ts showed differing susceptibility to H5N1 and non-zoonotic AIVs. Viral receptors expressed by HTEpC-Ts bound all viruses; however, the endosomal pH was associated with the overall susceptibility to infection by AIVs. Moreover, H5N1 hemagglutinin broadened viral tropism to include HTEpC-Ts, because it had a higher pH threshold for viral–cell membrane fusion. Thus, H5N1 viruses infect human tracheal epithelial cells as a result of their higher pH threshold for membrane fusion which may be one mechanism underlying H5N1 pathogenesis in human airway epithelia. Efficient replication of H5N1 in the conducting airways of humans may facilitate infection of the lower respiratory tract. Full article
(This article belongs to the Special Issue Evolution and Pathogenesis of Avian and Animal Influenza Viruses)
Open AccessArticle
The R251K Substitution in Viral Protein PB2 Increases Viral Replication and Pathogenicity of Eurasian Avian-like H1N1 Swine Influenza Viruses
Viruses 2020, 12(1), 52; https://doi.org/10.3390/v12010052 - 02 Jan 2020
Abstract
The Eurasian avian-like swine (EA) H1N1 virus has affected the Chinese swine industry, and human infection cases have been reported occasionally. However, little is known about the pathogenic mechanism of EA H1N1 virus. In this study, we compared the mouse pathogenicity of A/swine/Guangdong/YJ4/2014 [...] Read more.
The Eurasian avian-like swine (EA) H1N1 virus has affected the Chinese swine industry, and human infection cases have been reported occasionally. However, little is known about the pathogenic mechanism of EA H1N1 virus. In this study, we compared the mouse pathogenicity of A/swine/Guangdong/YJ4/2014 (YJ4) and A/swine/Guangdong/MS285/2017 (MS285) viruses, which had similar genotype to A/Hunan/42443/2015 (HuN-like). None of the mice inoculated with 106 TCID50 of YJ4 survived at 7 days post infection, while the survival rate of the MS285 group was 100%. Therefore, a series of single fragment reassortants in MS285 background and two rescued wild-type viruses were generated by using the reverse genetics method, and the pathogenicity analysis revealed that the PB2 gene contributed to the high virulence of YJ4 virus. Furthermore, there were 11 amino acid differences in PB2 between MS285 and YJ4 identified by sequence alignment, and 11 single amino acid mutant viruses were generated in the MS285 background. We found that the R251K mutation significantly increased the virulence of MS285 in mice, contributed to high polymerase activity and enhanced viral genome transcription and replication. These results indicate that PB2-R251K contributes to the virulence of the EA H1N1 virus and provide new insight into future molecular epidemiological surveillance strategies. Full article
(This article belongs to the Special Issue Evolution and Pathogenesis of Avian and Animal Influenza Viruses)
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