Equine Herpesvirus Pathogenesis and Immunology

Equine herpesviruses are a group of highly contagious pathogens that cause respiratory disease, abortion storms and neurological syndromes in equids worldwide. Infection typically begins with replication in the respiratory epithelium, followed by cell‐associated spread to local lymphoid tissues and subsequent viremia. The virus establishes lifelong latency in sensory ganglia and lymphoid cells, from which it can reactivate under stress, leading to recrudescent shedding and renewed transmission. Host defence relies on innate mucosal barriers and inflammatory mediators, including type I interferons, antimicrobial peptides and acute‐phase proteins, while adaptive immunity involves virus‐specific neutralising antibodies and cytotoxic T‐cell responses. Immunomodulatory viral proteins dampen host cytokine signalling, delay antigen presentation and interfere with leukocyte trafficking, contributing to disease severity and persistence. Recent advances have illuminated the molecular orchestration of immediate‐early, early and late viral gene expression, the role of oxidative stress pathways in infection, and the genetic determinants of neuropathogenicity. Improved understanding of these mechanisms underpins novel vaccine designs, antiviral therapies and surveillance strategies with global importance for equine health and biosecurity.

Research from Nature Portfolio

Recent studies employing long‐read nanopore transcriptomics have provided a detailed temporal map of host cell responses to EHV-1 infection. By quantifying direct cDNA reads at multiple time points, researchers identified six kinetic clusters of host genes, revealing coordinated upregulation of antiviral transcription factors in the immediate-early phase and modulation of late-phase pathways affecting cytoskeletal dynamics and metabolism. Network analysis uncovered putative transcriptional regulators driving these responses, while differential transcript usage analyses highlighted splice variants linked to immune signalling. These insights clarify how EHV-1 orchestrates host transcriptional reprogramming and suggest novel targets for therapeutic intervention.

Equine Herpesvirus Pathogenesis and Immunology publication trend

The graph below shows the total number of articles in equine herpesvirus pathogenesis and immunology across all publications each year (not limited to Nature Index journals).

Technical terms

Latency: A state in which the virus persists in host cells without producing infectious progeny, capable of reactivation under stress.

Viremia: The presence of virus particles in the bloodstream, facilitating systemic dissemination and infection of secondary sites.

DIVA (Differentiation of Infected and Vaccinated Animals): A vaccination strategy using marker genes to distinguish vaccinated individuals from naturally infected ones.

Immediate‐early genes: Viral genes expressed immediately upon infection that regulate subsequent phases of the viral replication cycle.

Mucosal immunity: Immune defences acting at mucosal surfaces, including antimicrobial peptides and local cytokine responses, that block pathogen entry and early replication.

References

1. EHV-1: A Constant Threat to the Horse Industry. Frontiers in Microbiology (2019).
2. A Point Mutation in a Herpesvirus Polymerase Determines Neuropathogenicity. PLOS Pathogens (2007).
3. Temporal transcriptional profiling of host cells infected by a veterinary alphaherpesvirus using nanopore sequencing. Scientific Reports (2025).
4. Development of a live attenuated vaccine candidate for equid alphaherpesvirus 1 control: a step towards efficient protection. Frontiers in Immunology (2024).
5. Immune horses rapidly increase antileukoproteinase and lack type I interferon secretion during mucosal innate immune responses against equine herpesvirus type 1. Microbiology Spectrum (2024).
6. Rutin prevents EqHV-8 induced infection and oxidative stress via Nrf2/HO-1 signaling pathway. Frontiers in Cellular and Infection Microbiology (2024).