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Influenza Viruses: Infection and Genomics
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Influenza Viruses: Infection and Genomics

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 20 October 2024 | Viewed by 5251

Special Issue Editor

Dr. Daniele Focosi

E-Mail
Guest Editor
Pisa University Hospital, 56126 Pisa, Italy
Interests: virology; emerging viruses; pandemics; viral evolution; hematology; immunogenetics; transplant immunology; transfusion medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

I am introducing here a Special Issue on influenza viruses. This Special Issue will cover all aspects of genomic, proteomics, and infection, including evolution, bioinformatic analyses, pathogenesis, and host responses.

The influenza virus has been known to pose a serious risk to human health since it was first identified in the 1930s. The influenza virus continues to resurface. To find new methods for both drug development and disease management, it is important to closely research the mechanisms of influenza virus replication, viral–host contact, and host defense/restriction responses. This Special Issue will focus on mechanisms underlying the spread of infection, virus load, escape of host defense, and modification of inflammatory response.

Contributions broadly related to the development of molecular biological processes in the cell following infection by the influenza virus are welcomed. In vitro reports and reviews on prophylactic and therapeutic agents are also encouraged. Since IJMS is a journal of molecular science, purely clinical studies will not be suitable. However, clinical or pure model submissions with biomolecular experiments are welcomed.

Dr. Daniele Focosi
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • influenza viruses
  • avian influenza
  • virus replication
  • infection
  • convergent evolution
  • restriction factors

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Published Papers (4 papers)

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Research

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14 pages, 13173 KiB  
Article
The Identification and Function of Linc01615 on Influenza Virus Infection and Antiviral Response
by Guihu Yin, Jianing Hu, Xiangyu Huang, Yiqin Cai, Zichen Gao, Xinyu Guo and Xiuli Feng
Int. J. Mol. Sci. 2024, 25(12), 6584; https://doi.org/10.3390/ijms25126584 - 14 Jun 2024
Viewed by 556
Abstract
Influenza virus infection poses a great threat to human health globally each year. Non-coding RNAs (ncRNAs) in the human genome have been reported to participate in the replication process of the influenza virus, among which there are still many unknowns about Long Intergenic [...] Read more.
Influenza virus infection poses a great threat to human health globally each year. Non-coding RNAs (ncRNAs) in the human genome have been reported to participate in the replication process of the influenza virus, among which there are still many unknowns about Long Intergenic Non-Coding RNAs (LincRNAs) in the cell cycle of viral infections. Here, we observed an increased expression of Linc01615 in A549 cells upon influenza virus PR8 infection, accompanied by the successful activation of the intracellular immune system. The knockdown of Linc01615 using the shRNAs promoted the proliferation of the influenza A virus, and the intracellular immune system was inhibited, in which the expressions of IFN-β, IL-28A, IL-29, ISG-15, MX1, and MX2 were decreased. Predictions from the catRAPID website suggested a potential interaction between Linc01615 and DHX9. Also, knocking down Linc01615 promoted influenza virus proliferation. The subsequent transcriptome sequencing results indicated a decrease in Linc01615 expression after influenza virus infection when DHX9 was knocked down. Further analysis through cross-linking immunoprecipitation and high-throughput sequencing (CLIP-seq) in HEK293 cells stably expressing DHX9 confirmed the interaction between DHX9 and Linc01615. We speculate that DHX9 may interact with Linc01615 to partake in influenza virus replication and that Linc01615 helps to activate the intracellular immune system. These findings suggest a deeper connection between DHX9 and Linc01615, which highlights the significant role of Linc01615 in the influenza virus replication process. This research provides valuable insights into understanding influenza virus replication and offers new targets for preventing influenza virus infections. Full article
(This article belongs to the Special Issue Influenza Viruses: Infection and Genomics)
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15 pages, 3119 KiB  
Article
Runx3 Regulates CD8+ T Cell Local Expansion and CD43 Glycosylation in Mice by H1N1 Influenza A Virus Infection
by Qin Hao, Suman Kundu, Sreerama Shetty and Hua Tang
Int. J. Mol. Sci. 2024, 25(8), 4220; https://doi.org/10.3390/ijms25084220 - 11 Apr 2024
Viewed by 1110
Abstract
We have recently reported that transcription factor Runx3 is required for pulmonary generation of CD8+ cytotoxic T lymphocytes (CTLs) that play a crucial role in the clearance of influenza A virus (IAV). To understand the underlying mechanisms, we determined the effects of [...] Read more.
We have recently reported that transcription factor Runx3 is required for pulmonary generation of CD8+ cytotoxic T lymphocytes (CTLs) that play a crucial role in the clearance of influenza A virus (IAV). To understand the underlying mechanisms, we determined the effects of Runx3 knockout (KO) on CD8+ T cell local expansion and phenotypes using an inducible general Runx3 KO mouse model. We found that in contrast to the lungs, Runx3 general KO promoted enlargement of lung-draining mediastinal lymph node (mLN) and enhanced CD8+ and CD4+ T cell expansion during H1N1 IAV infection. We further found that Runx3 deficiency greatly inhibited core 2 O-glycosylation of selectin ligand CD43 on activated CD8+ T cells but minimally affected the cell surface expression of CD43, activation markers (CD44 and CD69) and cell adhesion molecules (CD11a and CD54). Runx3 KO had a minor effect on lung effector CD8+ T cell death by IAV infection. Our findings indicate that Runx3 differently regulates CD8+ T cell expansion in mLNs and lungs by H1N1 IAV infection. Runx3 is required for CD43 core 2 O-glycosylation on activated CD8+ T cells, and the involved Runx3 signal pathway may mediate CD8+ T cell phenotype for pulmonary generation of CTLs. Full article
(This article belongs to the Special Issue Influenza Viruses: Infection and Genomics)
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9 pages, 1074 KiB  
Communication
Knockout of the Tnfa Gene Decreases Influenza Virus-Induced Histological Reactions in Laboratory Mice
by Darya A. Savenkova, Andrey S. Gudymo, Alexey N. Korablev, Oleg S. Taranov, Darya V. Bazovkina, Nataliya V. Danilchenko, Olga N. Perfilyeva, Elena K. Ivleva, Anastasiya A. Moiseeva, Yulia A. Bulanovich, Elena V. Roshchina, Irina A. Serova, Nariman R. Battulin, Elizabeth A. Kulikova and Dmitry V. Yudkin
Int. J. Mol. Sci. 2024, 25(2), 1156; https://doi.org/10.3390/ijms25021156 - 18 Jan 2024
Cited by 1 | Viewed by 1398
Abstract
Tumor necrosis factor alpha (TNF-α) is a cytokine that is responsible for many processes associated with immune response and inflammation. It is involved in the development of an antiviral response to many virus infections. This factor was shown to be activated in influenza [...] Read more.
Tumor necrosis factor alpha (TNF-α) is a cytokine that is responsible for many processes associated with immune response and inflammation. It is involved in the development of an antiviral response to many virus infections. This factor was shown to be activated in influenza A virus infection, which enhances production of other cytokines. The overexpression of these cytokines can lead to a cytokine storm. To study the role of TNF-α in the development of pathologies associated with viral infection, we generated a Tnfa knockout mouse strain. We demonstrated that these mice were characterized by a significant increase in the number of viral genomes compared to that in the parental strain, but the amount of live virus did not differ. A histopathology of the lungs in the genetically modified animals was significantly lower in terms of interalveolar septal infiltration. The generated model may be used to further study pathological processes in viral infections. Full article
(This article belongs to the Special Issue Influenza Viruses: Infection and Genomics)
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Review

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16 pages, 621 KiB  
Review
Avian Influenza Virus A(H5Nx) and Prepandemic Candidate Vaccines: State of the Art
by Daniele Focosi and Fabrizio Maggi
Int. J. Mol. Sci. 2024, 25(15), 8550; https://doi.org/10.3390/ijms25158550 - 5 Aug 2024
Viewed by 967
Abstract
Avian influenza virus has been long considered the main threat for a future pandemic. Among the possible avian influenza virus subtypes, A(H5N1) clade 2.3.4.4b is becoming enzootic in mammals, representing an alarming step towards a pandemic. In particular, genotype [...] Read more.
Avian influenza virus has been long considered the main threat for a future pandemic. Among the possible avian influenza virus subtypes, A(H5N1) clade 2.3.4.4b is becoming enzootic in mammals, representing an alarming step towards a pandemic. In particular, genotype B3.13 has recently caused an outbreak in US dairy cattle. Since pandemic preparedness is largely based on the availability of prepandemic candidate vaccine viruses, in this review we will summarize the current status of the enzootics, and challenges for H5 vaccine manufacturing and delivery. Full article
(This article belongs to the Special Issue Influenza Viruses: Infection and Genomics)
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