Equine herpesvirus battling with immune cells in a horse.

Equine Herpesvirus: How a Virus Triggers Abortion in Horses

Samir D’Costa in Health & Wellness December 2025 • 4 min read.

"Understanding EHV-1's strategy for evading the immune system could lead to better prevention."

Equine herpesvirus-1 (EHV-1) is a major threat to horses. It can cause everything from mild respiratory issues to late-term abortions and neurological problems. What makes EHV-1 so complex is that different strains behave differently. Some are more likely to cause abortions (abortigenic), while others lead to neurological issues (neurovirulent). Both types replicate in the lining of the upper respiratory tract, but abortigenic strains tend to form larger, more noticeable patches.

Scientists have been trying to figure out why these strains differ in their effects. One idea is that abortigenic strains might be better at dodging the horse's immune defenses, specifically the type I interferon response. Interferons are crucial proteins that help the body fight off viruses. If a virus can suppress or avoid this response, it could replicate more effectively and cause more severe disease.

This article delves into new research that explores how abortigenic and neurovirulent EHV-1 strains interact with the interferon response. By understanding these interactions, we can potentially develop better strategies to protect horses from the devastating effects of EHV-1.

Decoding EHV-1's Immune Evasion Tactics: What the Study Reveals

Equine herpesvirus battling with immune cells in a horse.

To investigate the interferon response, researchers used two models: primary respiratory epithelial cells (EREC) and respiratory mucosa explants (tissue samples) from horses. They infected these with both abortigenic and neurovirulent EHV-1 strains and then measured interferon alpha (IFNα) levels.

The study revealed a few key findings:

Interferon Production: Both types of EHV-1 triggered IFNα production in the respiratory tissues. There was no significant difference in the amount of interferon produced between the abortigenic and neurovirulent strains.
IFN Susceptibility: Pretreating cells with recombinant equine IFNα (rEqIFNα) suppressed the replication of both types of EHV-1. Conversely, blocking interferon signaling with Ruxolitinib (Rux) increased viral replication, indicating that both strain types are susceptible to interferon's antiviral effects.
Abortigenic Strain Anomaly: In a surprising twist, a moderate concentration of rEqIFNα (100 U/ml) actually increased the replication of abortigenic EHV-1 in some horses, compared to a lower concentration (10 U/ml). This effect wasn't seen with the neurovirulent strains.
Plaque Size Differences: When interferon signaling was blocked, the typically smaller viral plaques caused by neurovirulent strains became larger. However, the plaque size of abortigenic strains remained relatively unchanged.

These results suggest that while both types of EHV-1 trigger interferon production, the abortigenic strains might have developed unique mechanisms to counteract or even exploit the interferon response under certain conditions. This could explain why abortigenic strains replicate more efficiently in the upper respiratory tract.

What Does This Mean for Horse Owners?

This research highlights the crucial role of the interferon response in controlling EHV-1. It also suggests that abortigenic EHV-1 strains might have evolved ways to lessen the impact of interferon, potentially explaining their ability to cause more severe respiratory disease and abortions.

While more research is needed to fully understand these mechanisms, these findings open new doors for developing more effective prevention and treatment strategies. Potential avenues include:

<ul> <li>Targeted Vaccines: Designing vaccines that specifically boost the interferon response against abortigenic strains.</li> <li>Immunomodulatory Therapies: Developing therapies that fine-tune the interferon response to prevent the virus from exploiting it.</li> <li>Early Detection: Improving diagnostic tools for early detection of EHV-1, allowing for timely intervention and minimizing the risk of outbreaks.</li> </ul>

About this Article -

This article was crafted using a human-AI hybrid and collaborative approach. AI assisted our team with initial drafting, research insights, identifying key questions, and image generation. Our human editors guided topic selection, defined the angle, structured the content, ensured factual accuracy and relevance, refined the tone, and conducted thorough editing to deliver helpful, high-quality information.See our About page for more information.

This article is based on research published under:

DOI-LINK: 10.3389/fcimb.2018.00312, Alternate LINK

Title: Abortigenic But Not Neurotropic Equine Herpes Virus 1 Modulates The Interferon Antiviral Defense

Subject: Infectious Diseases

Journal: Frontiers in Cellular and Infection Microbiology

Publisher: Frontiers Media SA

Authors: Katrien C. K. Poelaert, Jolien Van Cleemput, Kathlyn Laval, Herman W. Favoreel, Gisela Soboll Hussey, Roger K. Maes, Hans J. Nauwynck

Published: 2018-09-12

Everything You Need To Know

What are the primary health risks associated with Equine Herpesvirus-1 (EHV-1) in horses?

Equine Herpesvirus-1 (EHV-1) poses a significant threat to horses as it leads to a spectrum of health issues. These range from relatively mild respiratory infections to severe consequences such as late-term abortions in pregnant mares and debilitating neurological disorders. The complexity of EHV-1 lies in the fact that different strains of the virus exhibit varying degrees of virulence, with some strains being more prone to inducing abortions (abortigenic) while others are more likely to cause neurological problems (neurovirulent).

How do abortigenic and neurovirulent strains of Equine Herpesvirus-1 (EHV-1) interact with the interferon response in horses, according to recent research?

Research indicates that both abortigenic and neurovirulent strains of Equine Herpesvirus-1 (EHV-1) trigger the production of interferon alpha (IFNα) in the respiratory tissues of horses. Interferons are crucial proteins that help the body fight off viruses. However, a notable finding is that abortigenic strains of EHV-1 might have developed mechanisms to counteract or even exploit the interferon response under certain conditions. This could explain why abortigenic strains replicate more efficiently in the upper respiratory tract and cause more severe respiratory disease and abortions. The study also revealed that blocking interferon signaling increased viral replication, indicating that both strain types are susceptible to interferon's antiviral effects.

What methods were used to investigate the interferon response to abortigenic and neurovirulent strains of Equine Herpesvirus-1 (EHV-1) in the recent study?

The study used primary respiratory epithelial cells (EREC) and respiratory mucosa explants (tissue samples) from horses. Researchers infected these with both abortigenic and neurovirulent EHV-1 strains and then measured interferon alpha (IFNα) levels. They also pretreated cells with recombinant equine IFNα (rEqIFNα) to suppress replication of both types of EHV-1 and blocked interferon signaling with Ruxolitinib (Rux) to increase viral replication. Plaque sizes were also measured in each of these conditions to see how the viral spread differed between strain types when the interferon response was active or blocked. These methodologies were chosen to directly observe how the different EHV-1 strains interact with the interferon response in relevant equine respiratory tissues.

What are the implications of research findings about interferon's role in EHV-1 for understanding why some infections lead to abortions?

The research suggests that abortigenic strains of Equine Herpesvirus-1 (EHV-1) may have developed unique ways to lessen the impact of interferon, potentially explaining their ability to cause more severe respiratory disease and abortions. While both abortigenic and neurovirulent strains trigger interferon production, the abortigenic strains might be able to counteract or even exploit the interferon response under certain conditions. This difference could be crucial in understanding why some EHV-1 infections lead to abortions while others result in neurological issues.

The study showed that a moderate concentration of interferon increased the replication of abortigenic EHV-1. What are the possible reasons for this anomaly and what was not addressed in the study?

The study showed a moderate concentration of recombinant equine IFNα (rEqIFNα) (100 U/ml) actually *increased* the replication of abortigenic EHV-1 in some horses, compared to a lower concentration (10 U/ml), whereas this was not seen with neurovirulent strains. The reason for this anomaly is not fully explained. The study did not focus on specific molecular mechanisms, which could explain how this occurs. Future research could explore specific genes or proteins that are differentially expressed or regulated in abortigenic strains in response to varying interferon concentrations. Identifying these factors could provide targets for new antiviral therapies.