Vaccines and Antiviral Drugs Against Viral Diseases in Domestic Animals

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Viral Immunology, Vaccines, and Antivirals".

Deadline for manuscript submissions: 31 July 2026 | Viewed by 2927

Special Issue Editor

State Key Laboratory for Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, China
Interests: immune evasion mechanisms of major domestic animal viruses; particularly PRRSV (porcine reproductive and respiratory syndrome virus) and FMDV (foot-and-mouth disease virus); as well as the development of marker vaccines, antiviral drugs and diagnostic methods for these pathogens

Special Issue Information

Dear Colleagues,

Viral diseases in domestic animals pose significant threats to global livestock health, agricultural productivity, and food security. The development and application of vaccines and antiviral drugs represent pivotal strategies in preventing and controlling these infections. While vaccines provide long-term immunity and reduce disease transmission, antiviral therapies offer critical tools for managing acute outbreaks and mitigating economic losses. However, challenges such as viral evolution, host–pathogen interactions, and the need for cost-effective solutions in diverse livestock systems demand continuous innovation. This Special Issue will highlight advances in vaccine technologies, the discovery of antiviral drugs, and their synergistic applications against viral pathogens affecting domestic animals.

We invite submissions of original research articles, reviews, and perspectives addressing (but not limited to) the following topics:

  • Novel vaccine platforms (e.g., mRNA, viral vectors, and subunit vaccines) for livestock viruses;
  • Antiviral drug development targeting viral entry, replication, or host immune modulation;
  • Combination strategies integrating vaccines and antivirals for enhanced disease control;
  • Immune correlates of protection and cross-species immunity in livestock vaccination;
  • Diagnostic tools to evaluate vaccine efficacy and antiviral drug resistance;
  • One Health approaches linking animal and human viral disease prevention;
  • Field applications of vaccines and antivirals in endemic or emerging outbreaks;
  • Viral evasion mechanisms and strategies to overcome them;
  • Next-generation technologies (e.g., CRISPR, AI-driven drug design, and nanotechnology) in veterinary virology.

This Special Issue will foster interdisciplinary collaboration among virologists, immunologists, pharmacologists, and veterinary scientists. Contributions including both fundamental research and translational applications are highly encouraged.

Dr. Jing Zhang
Guest Editor

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Keywords

  • vaccines
  • antiviral drugs
  • domestic animals
  • virus

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Published Papers (4 papers)

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Research

12 pages, 1833 KB  
Article
STING Degradation by PRRSV Activates HK2-Mediated Glycolysis to Facilitate Viral Replication
by Li Luo, Long Zhou, Xue Gao, Yuling Li, Han Zhou, Yanmin Li and Zhidong Zhang
Viruses 2026, 18(3), 284; https://doi.org/10.3390/v18030284 - 27 Feb 2026
Viewed by 160
Abstract
Porcine reproductive and respiratory syndrome virus (PRRSV) infection relies on glycolytic reprogramming to support replication, but the mechanisms driving this metabolic shift remain poorly understood. The stimulator of interferon genes (STING), an innate immune adaptor, recently emerged as a metabolic regulator by directly [...] Read more.
Porcine reproductive and respiratory syndrome virus (PRRSV) infection relies on glycolytic reprogramming to support replication, but the mechanisms driving this metabolic shift remain poorly understood. The stimulator of interferon genes (STING), an innate immune adaptor, recently emerged as a metabolic regulator by directly binding and inhibiting hexokinase-2 (HK2), a key rate-limiting enzyme in glycolysis. Whether PRRSV exploits the STING-HK2 axis to unleash glycolysis for its own replication is unknown. Here we demonstrate that PRRSV infection induced STING degradation and promoted HK2 suppression, activating glycolysis for viral replication. In PRRSV-infected Marc-145 cells, lactate production (a glycolysis marker) and HK2 expression increased time-dependently, peaking at 48 h post-infection (hpi). Conversely, STING protein levels decreased significantly at 36 hpi and further at 48 hpi, suggesting a correlation between STING downregulation and glycolytic activation. The HK2 inhibitor 2-deoxy-D-glucose reduced lactate production and viral load, while the glycolysis activator PS48 enhanced both. STING knockdown via siRNA increased HK2 expression, lactate secretion, and PRRSV nucleocapsid protein levels, whereas STING overexpression suppressed these phenotypes. Co-immunoprecipitation and confocal microscopy demonstrated direct STING-HK2 interaction and cytoplasmic co-localization, maintained during PRRSV infection. HK2 overexpression promoted viral replication without altering STING levels, confirming HK2 as a downstream effector. In conclusion, PRRSV-triggered degradation of STING enhances HK2 expression, promoting lactate accumulation and accelerating viral replication. These findings suggest that the STING-HK2 axis can act as a critical viral metabolic checkpoint and highlight targeting metabolic–immune crosstalk as a potential anti-viral strategy. Full article
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17 pages, 2908 KB  
Article
Assessment of Functional Antibody Responses Induced by Tembusu Virus Vaccines Using a Blocking ELISA
by Chengguang Lu, Siming Zhu, Wenjun Jiang, Mingtian Mao, Huihui Li, Bing Li, Meijuan Zhang, Mian Wu, Zhuo Zhang, Dalin He, Youxiang Diao and Yi Tang
Viruses 2026, 18(2), 256; https://doi.org/10.3390/v18020256 - 18 Feb 2026
Viewed by 304
Abstract
To establish a rapid, sensitive, and reproducible method for evaluating the immunogenic performance of Tembusu virus (TMUV) vaccines, we developed and optimized a blocking enzyme-linked immunosorbent assay (bELISA) using the TMUV envelope (E) protein as the coating antigen. By systematically screening the coating [...] Read more.
To establish a rapid, sensitive, and reproducible method for evaluating the immunogenic performance of Tembusu virus (TMUV) vaccines, we developed and optimized a blocking enzyme-linked immunosorbent assay (bELISA) using the TMUV envelope (E) protein as the coating antigen. By systematically screening the coating antigen concentration, mAb dilution, serum dilution, and chromogenic reaction time, we determined the optimal reaction conditions for this assay. The results showed that bELISA exhibited high specificity, yielding positive reactions only with TMUV-positive sera and no cross-reactivity with sera against other common duck viruses; the cutoff value for positivity was 48.89%, and the lowest detectable serum dilution was 1:10. Neutralization assays confirmed that the TMUV E-specific mAb significantly inhibited viral replication, supporting the functional relevance and reliability of the established bELISA. In a comparative investigation, this assay was used to assess five TMUV vaccines, including both inactivated and attenuated variants, in Cherry Valley ducks. The DF2 inactivated vaccine was found to elicit the highest antibody levels and blocking rates. This was followed by the WF100 attenuated vaccine, which also demonstrated a strong immune response. The TC2B inactivated vaccine, although effective, showed a comparatively lower response, whereas the FX2010-180P strain and mosquito cell-derived WF100 attenuated vaccine showed weaker immunogenicity. Neutralization assays further confirmed that the TMUV E-specific mAb significantly inhibited viral replication, supporting the functional relevance and reliability of the established bELISA. In summary, the bELISA described here demonstrates high specificity, sensitivity, and reproducibility and is suitable for evaluating the immune efficacy of different TMUV vaccines, providing a reliable technical platform for vaccine immunology studies and optimization of immunization strategies. Full article
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11 pages, 5428 KB  
Article
Evaluation of the Pathogenicity of Highly Virulent Eurasian Genotype II African Swine Fever Virus with MGF505-2R Gene Deletion in Piglets
by Fan Xu, Huaguo Huang, Wen Dang, Yu Du, Tao Li, Huanan Liu, Zhengwang Shi, Hong Tian, Jijun He and Haixue Zheng
Viruses 2025, 17(12), 1565; https://doi.org/10.3390/v17121565 - 29 Nov 2025
Viewed by 710
Abstract
African swine fever virus (ASFV) poses a significant threat to the global pig industry due to high mortality rates and complex genetic variation. Live attenuated vaccines (LAVs) provide protection against ASFV. Previously, MGF505-2R was identified as a potent inhibitor of innate immunity in [...] Read more.
African swine fever virus (ASFV) poses a significant threat to the global pig industry due to high mortality rates and complex genetic variation. Live attenuated vaccines (LAVs) provide protection against ASFV. Previously, MGF505-2R was identified as a potent inhibitor of innate immunity in vitro. This study evaluates the pathogenicity of a recombinant Eurasian genotype II strain with the MGF505-2R gene deleted (ASFV-ΔMGF505-2R) in piglets. Twelve five-week-old crossbred piglets were divided into two groups, with one group of eight piglets inoculated with ASFV-ΔMGF505-2R (n = 8) and the other group of four piglets inoculated with the same dose of parental ASFV CN/GS 2018 (n = 4). Clinical symptoms, viral loads, and immune responses were monitored over 30 days. ASFV-ΔMGF505-2R-inoculated piglets exhibited transient fever and low viremia only in the beginning of the challenge, while the control group developed high levels of viremia and hyperthermia at day 2 and 8 post-challenge, respectively. Meanwhile, the control group demonstrated more severe post-mortem signs and immuno-histochemistry injury when compared to the ΔMGF505-2R group. ELISA analysis displayed higher levels of IFN-β and IL-1β in the ΔMGF505-2R group, further solidating the immunosuppressive role of MGF505-2R. All ASFV-ΔMGF505-2R-inoculated piglets developed high titers of ASFV-specific P30 antibodies at 10 days post-challenge. These findings rationalized the potential of ASFV-ΔMGF505-2R as a live attenuated candidate for ASF infection. Full article
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14 pages, 2139 KB  
Article
Phospholipase PLA2G16 Accelerates the Host Interferon Signaling Pathway Response to FMDV
by Bingjie Sun, Xiaodong Qin, Taoqing Zhang, Sujie Dong, Yinbo Ye, Changying Wang, Yan Zhang, Rongzeng Hao, Yi Ru, Hong Tian and Haixue Zheng
Viruses 2025, 17(7), 883; https://doi.org/10.3390/v17070883 - 23 Jun 2025
Cited by 1 | Viewed by 1153
Abstract
PLA2G16 is a member of the phospholipase A2 family that catalyzes the generation of lysophosphatidic acids (LPAs) and free fatty acids (FFAs) from phosphatidic acid. Previously, PLA2G16 was found to be a host factor for picornaviruses. Here, we discovered that the Foot-and-Mouth Disease [...] Read more.
PLA2G16 is a member of the phospholipase A2 family that catalyzes the generation of lysophosphatidic acids (LPAs) and free fatty acids (FFAs) from phosphatidic acid. Previously, PLA2G16 was found to be a host factor for picornaviruses. Here, we discovered that the Foot-and-Mouth Disease Virus (FMDV) infection led to an elevation in PLA2G16 transcription. We established PLA2G16 overexpression and knockdown cell lines in PK-15 cells to investigate the potential role of PLA2G16 in FMDV infection. Our findings revealed that during FMDV infection, PLA2G16-overexpressing cells had increased levels of phosphorylated STAT1 and the interferon-stimulating factors ISG15 and ISG56. In PLA2G16-overexpressing cells, p-STAT1 was observed at higher levels and earlier than in wild-type cells. Subsequent research demonstrated that PLA2G16 specifically promoted an antiviral innate immune response against FMDV. The host could detect the early release of FMDV viral nucleic acid in PLA2G16-overexpressing cells and trigger the interferon signaling pathway. Additionally, we discovered that the supernatants of PLA2G16-overexpressing cells stimulated the production of higher levels of ISG56 and phosphorylated STAT1. This suggests that PLA2G16-overexpressing cells can activate the innate immune pathway of uninfected cells after FMDV infection. Full article
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