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Immune Cell Signaling in Feline Infectious Peritonitis Virus Infection and Implications for Vaccine Design
1College of Veterinary Medicine, Chungnam National University, Daejeon 34134, Republic of Korea.
Vaccines
|May 26, 2026
Summary
Developing a safe and effective vaccine for feline infectious peritonitis virus (FIPV) requires understanding host immune responses. New strategies must limit inflammation and macrophage activation to prevent disease enhancement.
Area of Science:
- Veterinary Virology
- Immunology
- Vaccine Development
Background:
- Feline infectious peritonitis virus (FIPV) causes a challenging disease with no consistently effective vaccine.
- Disease severity depends on host immune responses, particularly macrophage and monocyte signaling, leading to immunopathology.
- Previous FIPV vaccines have shown inconsistent protection and sometimes enhanced disease.
Purpose of the Study:
- To review current knowledge of immune cell signaling pathways in FIPV infection.
- To explore how these pathways influence vaccine-induced immunity.
- To propose reframed vaccine development strategies for FIPV.
Main Methods:
- Review of literature on immune signaling pathways (Toll-like receptors, MAPKs, NF-κB, cytokines, Fc receptors, autophagy) in FIPV.
- Integration of data on immune signaling kinetics, antibody functionality, adjuvant effects, and platform-specific immune signatures.
- Analysis of how these mechanisms shape vaccine-induced immunity.
Main Results:
- FIPV disease severity is linked to excessive inflammation driven by macrophage and monocyte signaling.
- Vaccine-induced immune responses mimicking pathogenic pathways can exacerbate disease.
- Understanding specific immune signaling pathways is crucial for effective FIPV vaccine design.
Conclusions:
- Future FIPV vaccine development should focus on modulating host immune responses rather than solely maximizing immunogenicity.
- Strategies should aim to limit sustained macrophage activation and pro-inflammatory cytokine amplification.
- This approach may reduce antibody-dependent enhancement and immunopathology, offering broader lessons for vaccine design.

