Viral Load and Cell Tropism During Early Latent Equid Herpesvirus 1 Infection Differ Over Time in Lymphoid and Neural Tissue Samples From Experimentally Infected Horses.
Authors: Giessler Kim S, Samoilowa Susanna, Soboll Hussey Gisela, Kiupel Matti, Matiasek Kaspar, Sledge Dodd G, Liesche Friederike, Schlegel Jürgen, Fux Robert, Goehring Lutz S
Journal: Frontiers in veterinary science
Summary
# Editorial Summary: EHV-1 Latency Establishment in Neural and Lymphoid Tissues Understanding how equid herpesvirus 1 establishes and maintains latency is crucial for managing recurrent respiratory disease and neurological complications in horses, yet the cellular mechanisms underlying this process remain poorly characterised. Researchers experimentally infected yearling horses intranasally with EHV-1 and collected neural and lymphoid tissue samples at 30 and 70 days post-infection, using quantitative PCR, in situ hybridisation, immunohistochemistry and reverse transcriptase PCR to map viral persistence and identify infected cell types. Viral DNA was detected in trigeminal ganglia, sympathetic trunk, and multiple lymph nodes at both timepoints, though copy numbers and positive sample rates declined significantly between day 30 and day 70; crucially, viral replication was absent (ruling out active infection), and by day 70, latent virus was localised exclusively within neurons rather than surrounding support cells. These findings suggest EHV-1 exploits an alternative route to establish latency via infected T-lymphocytes during viraemia, rather than relying solely on retrograde neuronal transport, potentially mirroring the behaviour of varicella-zoster virus in humans. For equine practitioners, this research illuminates why managing systemic immune status and controlling secondary viremia may be as important as monitoring neurological signs when treating EHV-1 infections—and hints at why certain horses may be predisposed to recrudescence despite apparent clinical recovery.
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Practical Takeaways
- •EHV-1 latency establishment occurs progressively over 70 days with dynamic changes in viral location and cellular tropism, which may inform timing of therapeutic interventions
- •Detection of latent virus in abdominal lymphoid tissues indicates systemic latency beyond neural ganglia, suggesting need for monitoring beyond respiratory tract signs
- •The T-cell mediated pathway to latency highlights the potential importance of immune function management in controlling EHV-1 reactivation risk
Key Findings
- •Viral DNA detected in trigeminal ganglia, sympathetic trunk, and lymph nodes at both 30 and 70 days post-infection, with significant decline in copy number over time
- •At 30 dpi, EHV-1 signal localized in both neurons and non-neuronal cells; at 70 dpi, signal restricted primarily to neurons in trigeminal ganglia
- •No evidence of lytic viral replication detected; mild inflammation with CD3+ T-lymphocyte infiltrates surrounding neuronal cell bodies
- •Results suggest EHV-1 establishes latency via both retrograde neuronal transport and T-cell-mediated viremia pathway, similar to Varicella Zoster Virus