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Pathogens
Special Issues
Replication and Pathogenesis of Influenza Viruses
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Replication and Pathogenesis of Influenza Viruses

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Emerging Pathogens".

Deadline for manuscript submissions: 20 March 2025 | Viewed by 6550

Special Issue Editor

Dr. Shih-Yen Lo

E-Mail Website
Guest Editor
Department of Laboratory Medicine and Biotechnology, Tzu Chi University, Hualien 97004, Taiwan
Interests: influenza A virus; hepatitis C virus; coronaviruses; translational control; viral replication; virus-host interactions
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Influenza viruses are able to cause seasonal influenza epidemics and even pandemics (e.g., 2009 Influenza A virus (novel H1N1)). Even with the availability of seasonal influenza vaccines and antiviral agents, seasonal epidemics caused by influenza viruses still result in 3 to 5 million severe cases, particularly among infants and older adults, and thousands of deaths globally each year. Therefore, more studies on the influenza viral life cycle, including cross-species transmission, are necessary.

The Special Issue will highlight recent advances in the mechanistic understanding of the replication and pathogenesis of influenza viruses. Both reviews and research articles are welcome. Topics can include but are not limited to the following:

  1. Expressional regulation and functional characterization of various viral gene products;
  2. Replication and pathogenesis of various influenza viruses;
  3. Interactions between influenza viruses and other pathogens (other viruses or bacteria);
  4. Interactions between influenza viruses and host cells, including antiviral immune responses;
  5. Countermeasures to combat influenza viral infection (e.g., vaccine development and antiviral agents).

Dr. Shih-Yen Lo
Guest Editor

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 submissions that pass pre-check are 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. Pathogens 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 2200 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

  • human influenza virus
  • avian influenza viruses
  • cross-species transmission
  • viral gene products
  • viral replication
  • virus–host interactions
  • viral pathogenesis
  • pathogen–pathogen interactions
  • antiviral immune responses
  • vaccine development
  • antiviral agents

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (2 papers)

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Research

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17 pages, 18102 KiB  
Article
Interactome Profiling of N-Terminus-Truncated NS1 Protein of Influenza A Virus Reveals Role of 14-3-3γ in Virus Replication
by Rei-Lin Kuo, Ee-Hong Tam, Chian-Huey Woung, Chu-Mi Hung, Hao-Ping Liu, Helene Minyi Liu and Chih-Ching Wu
Pathogens 2022, 11(7), 733; https://doi.org/10.3390/pathogens11070733 - 27 Jun 2022
Viewed by 2353
Abstract
Influenza A virus is transmitted through a respiratory route and has caused several pandemics throughout history. The NS1 protein of influenza A virus, which consists of an N-terminal RNA-binding domain and a C-terminal effector domain, is considered one of the critical virulence factors [...] Read more.
Influenza A virus is transmitted through a respiratory route and has caused several pandemics throughout history. The NS1 protein of influenza A virus, which consists of an N-terminal RNA-binding domain and a C-terminal effector domain, is considered one of the critical virulence factors during influenza A virus infection because the viral protein can downregulate the antiviral response of the host cell and facilitate viral replication. Our previous study identified an N-terminus-truncated NS1 protein that covers the C-terminus effector domain. To comprehensively explore the role of the truncated NS1 in cells, we conducted immunoprecipitation coupled with LC-MS/MS to identify its interacting cellular proteins. There were 46 cellular proteins identified as the components of the truncated NS1 protein complex. As for our previous results for the identification of the full-length NS1-interacting host proteins, we discovered that the truncated NS1 protein interacts with the γ isoform of the 14-3-3 protein family. In addition, we found that the knockdown of 14-3-3γ in host cells reduced the replication of the influenza A/PR8 wild-type virus but not that of the PR8-NS1/1-98 mutant virus, which lacks most of the effector domain of NS1. This research highlights the role of 14-3-3γ, which interacts with the effector domain of NS1 protein, in influenza A viral replication. Full article
(This article belongs to the Special Issue Replication and Pathogenesis of Influenza Viruses)
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Review

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19 pages, 2218 KiB  
Review
Strategies of Influenza A Virus to Ensure the Translation of Viral mRNAs
by Hui-Chun Li, Chee-Hing Yang and Shih-Yen Lo
Pathogens 2022, 11(12), 1521; https://doi.org/10.3390/pathogens11121521 - 12 Dec 2022
Cited by 5 | Viewed by 3517
Abstract
Viruses are obligatorily intracellular pathogens. To generate progeny virus particles, influenza A viruses (IAVs) have to divert the cellular machinery to ensure sufficient translation of viral mRNAs. To this end, several strategies have been exploited by IAVs, such as host gene shutoff, suppression [...] Read more.
Viruses are obligatorily intracellular pathogens. To generate progeny virus particles, influenza A viruses (IAVs) have to divert the cellular machinery to ensure sufficient translation of viral mRNAs. To this end, several strategies have been exploited by IAVs, such as host gene shutoff, suppression of host innate immune responses, and selective translation of viral mRNAs. Various IAV proteins are responsible for host gene shutoff, e.g., NS1, PA-X, and RdRp, through inhibition of cellular gene transcription, suppression of cellular RNA processing, degradation of cellular RNAs, and blockage of cellular mRNA export from the nucleus. Host shutoff should suppress the innate immune responses and also increase the translation of viral mRNAs indirectly due to the reduced competition from cellular mRNAs for cellular translational machinery. However, many other mechanisms are also responsible for the suppression of innate immune responses by IAV, such as prevention of the detection of the viral RNAs by the RLRs, inhibition of the activities of proteins involved in signaling events of interferon production, and inhibition of the activities of interferon-stimulated genes, mainly through viral NS1, PB1-F2, and PA-X proteins. IAV mRNAs may be selectively translated in favor of cellular mRNAs through interacting with viral and/or cellular proteins, such as NS1, PABPI, and/or IFIT2, in the 5′-UTR of viral mRNAs. This review briefly summarizes the strategies utilized by IAVs to ensure sufficient translation of viral mRNAs focusing on recent developments. Full article
(This article belongs to the Special Issue Replication and Pathogenesis of Influenza Viruses)
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