The Host Response to Animal Virus Infection

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Veterinary Microbiology".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 1449

Special Issue Editor


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Guest Editor
Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Beijing, China
Interests: porcine reproductive and respiratory syndrome virus; non-coding RNA; virus-host interactions
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Special Issue Information

Dear Colleagues,

Virus infection has caused tremendous amounts of economic losses to the animal husbandry industry worldwide, especially for respiratory virus, coronavirus, influenza virus, and newly emerging viral pathogens. The viruses have evolved to equip various strategies to disrupt the host immune response and provide favorable conditions for survival. The limited therapeutic options and vaccines currently available also impose an additional, significant burden on disease control and prevention.

A significant amount of information is necessary regarding virus–host interactions during infection. Efficient viral strategies for modulations of cellular processes include innate immunity, apoptosis, non-coding RNAs, inflammatory cytokines, and other cellular pathways. There is an urgent need for further basic research on the various biological stages of the virus within the host immune response that ensues in order to recognize potential therapeutic targets and design efficient antiviral drugs and vaccines.

This Special Issue of Microorganisms aspires to provide further insight into the challenges posed by animal virus infections in host immune response, pathogenesis, and therapy.

Dr. Liwei Li
Guest Editor

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Keywords

  • respiratory virus
  • coronavirus
  • emerging pathogens in animals
  • host immune response
  • innate immunity
  • neutralizing antibody
  • non-coding RNA
  • viral infection
  • antiviral agents
  • antiviral strategy

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Published Papers (2 papers)

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Research

17 pages, 8700 KB  
Article
Designing a Novel Multi-Epitope Trivalent Vaccine Against NDV, AIV and FAdV-4 Based on Immunoinformatics Approaches
by Jiashuang Ji, Xiaofeng Dong, Xiangyi Liu, Mengchun Ding, Yating Lin, Yunhang Zhang, Wuchao Zhang, Baishi Lei, Wanzhe Yuan and Kuan Zhao
Microorganisms 2025, 13(12), 2744; https://doi.org/10.3390/microorganisms13122744 - 2 Dec 2025
Viewed by 139
Abstract
The diseases caused by genotype VII Newcastle disease virus (NDV), H9N2 avian influenza virus (AIV), and fowl adenovirus serotype 4 (FAdV-4) continue to threaten the global poultry industry. However, no broad-spectrum vaccines provide simultaneous protection against these three pathogens. This study employed bioinformatics [...] Read more.
The diseases caused by genotype VII Newcastle disease virus (NDV), H9N2 avian influenza virus (AIV), and fowl adenovirus serotype 4 (FAdV-4) continue to threaten the global poultry industry. However, no broad-spectrum vaccines provide simultaneous protection against these three pathogens. This study employed bioinformatics and immunoinformatics approaches to design a multi-epitope vaccine, named NFAF, which consists of B-cell, cytotoxic T lymphocyte (CTL) epitopes, and helper T lymphocyte (HTL) epitopes derived from hemagglutinin-neuraminidase (HN) and fusion (F) proteins of genotype VII NDV, hemagglutinin (HA) protein of H9N2, and Fiber2 protein of FAdV-4. The vaccine candidate was predicted to have non-allergenic properties, non-toxicity, high antigenicity, and favorable solubility. Each of its constituent antigenic epitopes has a high degree of conservation. Molecular docking demonstrated stable binding between NFAF and chicken Toll-like receptor (TLRs) and major histocompatibility complex (MHC) molecules. NFAF was expressed in soluble form in Escherichia coli and purified. Polyclonal antibodies against all three target viruses showed specific binding to NFAF. In vitro experiments revealed that NFAF effectively stimulated chicken peripheral blood mononuclear cells (PBMCs) and induced Th1, Th2, and pro-inflammatory cytokine production, confirming its immunogenicity, and increased the mRNA expression of the key signaling molecules MyD88 and NF-κB. These results suggested that NFAF could therefore be an efficacious multi-epitope vaccine against genotype VII NDV, H9N2, and FAdV-4 infections. Full article
(This article belongs to the Special Issue The Host Response to Animal Virus Infection)
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19 pages, 3584 KB  
Article
PRV Induces Neurological Inflammatory Injury by Activating Necroptosis of Brain Tissue
by Chunzi Peng, Jinwu Zhang, Changxu Wu, Danning Liu, Jing Liang, Maojie Lv, Shisen Yang, Xiaoning Li, Yingyi Wei, Hailan Chen, Jiakang He, Tingjun Hu and Meiling Yu
Microorganisms 2025, 13(7), 1531; https://doi.org/10.3390/microorganisms13071531 - 30 Jun 2025
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Abstract
Pseudorabies virus (PRV) can infect a wide range of animal species, including swine and rodents. Infection in pigs is associated with significant economic losses in the global pork industry and is characterized by acute, often fatal disease, as well as central nervous system [...] Read more.
Pseudorabies virus (PRV) can infect a wide range of animal species, including swine and rodents. Infection in pigs is associated with significant economic losses in the global pork industry and is characterized by acute, often fatal disease, as well as central nervous system (CNS) invasion, which leads to neurological manifestations. Although PRV replication has been extensively characterized in certain murine neuronal cell lines such as Neuro-2a, the mechanisms underlying PRV-induced neuroinflammatory injury and necroptosis remain largely unclear. In this study, Kunming mice and mouse astrocytes (C8-D1A) were infected with PRV-GXLB-2013 at different doses to evaluate neurological injury and inflammatory responses. Given that the NF-κB/MLKL signaling pathway was found to be activated during PRV infection, a selective MLKL inhibitor, necrosulfonamide (NSA), was applied to investigate the role of necroptosis in PRV-induced neuroinflammatory damage. Mice infected with higher viral doses showed increased mortality, severe neurological symptoms, elevated brain inflammation, and pathological changes. In C8-D1A cells, PRV infection significantly upregulated inflammatory cytokines and key components of the NF-κB/MLKL pathway. Importantly, NSA treatment markedly reduced these inflammatory responses, mitochondrial damage, and cellular necrosis. Collectively, these findings suggest that PRV infection triggers neuroinflammatory injury through the activation of necroptosis and the NF-κB/MLKL signaling pathway. This study provides novel mechanistic insights into PRV-induced neurological damage and highlights potential therapeutic targets for intervention. Full article
(This article belongs to the Special Issue The Host Response to Animal Virus Infection)
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