Advance in Influenza A and Influenza B Viruses

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

Deadline for manuscript submissions: 30 September 2024 | Viewed by 2961

Special Issue Editor


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Guest Editor
Allergy and Clinical Immunology, National Institute for Occupational Health and Safety, Morgantown, WV, USA
Interests: RNA-viruses; host–virus interactions; Influenza virus; innate immunity; microRNA; gene regulation; emerging diseases; RSV; Rhino virus; emerging viruses; SARS-CoV-2

Special Issue Information

Dear Colleagues,

In humans, influenza viruses continue to cause significant morbidity and mortality annually. There are four types of influenza viruses (namely, A, B, C, and D), and in recent years influenza A and B viruses have been among the most reported viruses causing illness in humans. Seasonal influenza virus infection and its severity mostly depend on the circulating influenza virus strains. The recurring infection by less severe to fatal strains of influenza virus proves the limitations of our knowledge concerning the infectivity of both A and B influenza viruses. Influenza B virus infection is less common than influenza A, but studies have shown that influenza B infection can be severe in children. 

Influenza virus exposure activates both innate and adaptive immune responses to protect the cells against the virus attack. One of the major antiviral responses is through the elicitation of chemokines and cytokines by the human body during influenza infection. If there is an imbalance in the recruitment of neutrophils and monocytes to the site of infection, there can be an increase in cytokine expression that results in unwarranted inflammation in the lungs. NK and T cells contribute to innate immunity through cytotoxic activity, and their activation and inactivation by influenza viruses might be vital.

To develop novel prevention strategies, there is an urgent need to improve our understanding of the influenza virus, its immunomodulatory mechanisms in the host, and how influenza viruses adapt to this immune pressure. Researchers are coming up with new information in this field in order to understand the virology of different influenza viruses and help in dissecting the resulting host innate and adaptive immune responses following infection. This Special Issue of Pathogens is calling for research articles, review articles and short communications related to the molecular immunology, virus–host interaction, development of new antivirals and vaccines, diagnostics and epidemiology, and any other aspects of both influenza A and B viruses. We look forward to your contribution.

Dr. Sreekumar Othumpangat
Guest Editor

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Keywords

  • influenza A virus
  • influenza B virus
  • viral life cycle
  • virus-host interaction
  • antivirals
  • vaccine
  • epidemiology
  • molecular immunology

Published Papers (2 papers)

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Research

13 pages, 1748 KiB  
Article
Phylodynamic and Evolution of the Hemagglutinin (HA) and Neuraminidase (NA) Genes of Influenza A(H1N1) pdm09 Viruses Circulating in the 2009 and 2023 Seasons in Italy
by Fabio Scarpa, Leonardo Sernicola, Stefania Farcomeni, Alessandra Ciccozzi, Daria Sanna, Marco Casu, Marco Vitale, Alessia Cicenia, Marta Giovanetti, Chiara Romano, Francesco Branda, Massimo Ciccozzi and Alessandra Borsetti
Pathogens 2024, 13(4), 334; https://doi.org/10.3390/pathogens13040334 - 17 Apr 2024
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Abstract
The influenza A(H1N1) pdm09 virus, which emerged in 2009, has been circulating seasonally since then. In this study, we conducted a comprehensive genome-based investigation to gain a detailed understanding of the genetic and evolutionary characteristics of the hemagglutinin (HA) and neuraminidase (NA) surface [...] Read more.
The influenza A(H1N1) pdm09 virus, which emerged in 2009, has been circulating seasonally since then. In this study, we conducted a comprehensive genome-based investigation to gain a detailed understanding of the genetic and evolutionary characteristics of the hemagglutinin (HA) and neuraminidase (NA) surface proteins of A/H1N1pdm09 strains circulating in Italy over a fourteen-year period from 2009 to 2023 in relation to global strains. Phylogenetic analysis revealed rapid transmission and diversification of viral variants during the early pandemic that clustered in clade 6B.1. In contrast, limited genetic diversity was observed during the 2023 season, probably due to the genetic drift, which provides the virus with a constant adaptability to the host; furthermore, all isolates were split into two main groups representing two clades, i.e., 6B.1A.5a.2a and its descendant 6B.1A.5a.2a.1. The HA gene showed a faster rate of evolution compared to the NA gene. Using FUBAR, we identified positively selected sites 41 and 177 for HA and 248, 286, and 455 for NA in 2009, as well as sites 22, 123, and 513 for HA and 339 for NA in 2023, all of which may be important sites related to the host immune response. Changes in glycosylation acquisition/loss at prominent sites, i.e., 177 in HA and 248 in NA, should be considered as a predictive tool for early warning signs of emerging pandemics, and for vaccine and drug development. Full article
(This article belongs to the Special Issue Advance in Influenza A and Influenza B Viruses)
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21 pages, 6819 KiB  
Article
β-Defensin-1 Regulates Influenza Virus Infection in Human Bronchial Epithelial Cells through the STAT3 Signaling Pathway
by Sreekumar Othumpangat and John D. Noti
Pathogens 2023, 12(1), 123; https://doi.org/10.3390/pathogens12010123 - 11 Jan 2023
Cited by 4 | Viewed by 2043
Abstract
Understanding the host response to influenza A virus (IAV) infection is vital for developing intervention strategies. The primary barriers for invading respiratory pathogens are the respiratory tract epithelial cells and antimicrobial proteins generated by these cells. The antimicrobial peptide, β-defensin-1, has antiviral activity [...] Read more.
Understanding the host response to influenza A virus (IAV) infection is vital for developing intervention strategies. The primary barriers for invading respiratory pathogens are the respiratory tract epithelial cells and antimicrobial proteins generated by these cells. The antimicrobial peptide, β-defensin-1, has antiviral activity against both enveloped and non-enveloped viruses. Significant downregulation of β-defensin1 gene (DEFB1) expression was observed when human bronchial epithelial cells (HBEpCs) were exposed to IAV. HBEpCs overexpressing DEFB1 caused a significant reduction in IAV, that was confirmed by IAV matrix gene analysis, plaque assay, and confocal microscopy. DEFB1 expression after transfection with two micro RNAs (miRNAs), hsa-miR-186-5p and hsa-miR-340-5p, provided evidence that DEFB1 expression could be modulated by these miRNAs and hsa-miR-186-5p had a higher binding efficiency with DEFB1. Overexpression of DEFB1 in IAV-infected HBEpCs led to increased NF-κB expression. In a PCR array analysis of 84 transcription factors, either overexpressing DEFB1 or siRNA silencing of DEFB1 expression significantly modulated the expression of signal transducer and activator of transcription 3 (STAT3). In addition, Ingenuity Pathway Analysis (IPA) integrated with PCR array data showed that the JAK1/STAT3 pathway was significantly altered in cells overexpressing DEFB1, suggesting this to be one of the pathways by which defensin regulates IAV replication in HBEpCs. In conclusion, the reduction in IAV copy number in DEFB1 overexpressing cells suggests that β-defensin-1 plays a key role in regulating IAV survival through STAT3 and is a potential target for antiviral drug development. Full article
(This article belongs to the Special Issue Advance in Influenza A and Influenza B Viruses)
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