Equine Arteritis Virus Dynamics and Pathogenesis

Equine arteritis virus (EAV) is an enveloped positive-sense RNA virus within the Arteriviridae family that causes equine viral arteritis, a disease characterised by respiratory distress, systemic vasculitis and reproductive impairment. Infection commonly begins in the respiratory tract, with virus replication in alveolar macrophages and endothelial cells leading to viraemia and dissemination to multiple organs. In adult stallions, EAV may establish a long-term persistent infection within the accessory sex glands, resulting in continual viral shedding in semen. This persistence is underpinned by intricate host–virus interactions, including exploitation of chemokine pathways to modulate lymphocyte homing, dysregulation of CD8+ T-cell effector functions and the generation of diverse viral quasispecies that facilitate immune evasion. Viral tropism for reproductive tract tissues and the influence of host genetic factors—most notably allelic variants of the CXCL16 gene—determine the probability of chronic carriage. The global distribution of EAV and its economic impact on the equine breeding industry underscore the importance of integrated control measures, combining strategic vaccination, targeted surveillance of carrier stallions and rapid molecular diagnostics to interrupt transmission chains.

Research from Nature Portfolio

Recent studies have monitored the spread and genetic variability of EAV within native horse populations, revealing high seroprevalence rates in certain breeding groups and a striking degree of sequence conservation among field strains. Whole-genome sequencing of viral isolates from stallion semen demonstrated nucleotide identities exceeding ninety-five per cent, while deep sequencing uncovered extensive within-host variation, with dozens to hundreds of single-nucleotide variants co-existing as viral quasispecies. Analysis of host genetics in these cohorts confirmed that stallions carrying specific EqCXCL16 alleles are more likely to become persistent shedders, emphasising the interplay between viral evolution and host susceptibility. These findings highlight the necessity for ongoing genomic surveillance to detect emergent variants with altered pathogenic potential and to inform biosecurity strategies in diverse equine populations.

Research from all publishers

Transcriptomic profiling of the stallion ampullae has elucidated key immunopathogenic mechanisms underlying long-term EAV persistence. In persistent carriers, CD8+ T lymphocytes display an altered transcriptional signature dominated by the transcription factors EOMES and NFATC2, alongside upregulated inhibitory receptors. Concomitant overexpression of the CXCL16 chemokine and its receptor CXCR6 suggests that the CXCL16/CXCR6 axis drives aberrant lymphocyte trafficking and creates an immunoregulatory niche favouring viral survival. Foundational genetic studies have identified three allelic variants of the equine CXCL16 gene, one of which encodes a protein isoform that serves as a cellular receptor for EAV and correlates strongly with the establishment of long-term carrier status. This receptor-mediated entry mechanism provides a molecular basis for T-cell susceptibility and offers a target for genotype-guided management of breeding stallions. Additionally, an outbreak investigation in a show stallion population revealed that acute respiratory transmission can occur via aerosolised seminal fluids, underlining the potential for horizontal spread beyond direct breeding and calling for heightened biosecurity when introducing seronegative horses into mixed groups.

Equine Arteritis Virus Dynamics and Pathogenesis publication trend

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

Technical terms

Equine arteritis virus (EAV): An enveloped positive-sense RNA virus of the family Arteriviridae that infects horses and related species, causing viral arteritis.

Persistent infection: A prolonged state in which virus replicates at low levels within host tissues, often accompanied by intermittent or continuous shedding without overt disease signs.

Quasispecies: A complex, dynamic population of genetically related viral variants arising from high mutation rates during RNA replication within a single host.

CXCL16/CXCR6 axis: A chemokine-receptor pair that regulates lymphocyte homing and inflammatory responses, exploited by EAV to modulate local immunity.

Allelic variation: Differences in nucleotide sequences of a gene among individuals, which can alter protein function and influence susceptibility to infection.

Horizontal transmission: Spread of a pathogen between individuals by non-vertical routes, such as respiratory droplets or contaminated secretions, rather than from parent to offspring.

References

1. Equine arteritis virus long-term persistence is orchestrated by CD8+ T lymphocyte transcription factors, inhibitory receptors, and the CXCL16/CXCR6 axis. PLOS Pathogens (2019).
2. Allelic Variation in CXCL16 Determines CD3+ T Lymphocyte Susceptibility to Equine Arteritis Virus Infection and Establishment of Long-Term Carrier State in the Stallion. PLOS Genetics (2016).
3. Spread of equine arteritis virus among Hucul horses with different EqCXCL16 genotypes and analysis of viral quasispecies from semen of selected stallions. Scientific Reports (2020).
4. Equine Arteritis Virus (EAV) Outbreak in a Show Stallion Population. Viruses (2021).