Equine herpesvirus 1

What it is

Equine herpesvirus 1 (EHV-1, Equid alphaherpesvirus 1) is a widespread alphaherpesvirus. Most horses are infected as foals and the virus becomes latent in the trigeminal ganglion and in lymphocytes of lymphoid tissues; stress (transport, competition, weaning, illness) can reactivate it, and the horse sheds it from the nose again.

After multiplying in the respiratory epithelium, the virus enters blood leucocytes (cell-associated viraemia), which carry it to the endothelium of the small vessels of the pregnant uterus and the central nervous system. There it causes vasculitis and thrombosis, and the loss of blood supply produces the severe forms:

• Abortion in the last third of pregnancy, or the birth of weak foals that die within a few days.
• Equine herpesvirus myeloencephalopathy (EHM): ischaemic lesions mainly in the spinal cord and, to a lesser degree, in the brain.

A variant in the viral polymerase (the D752 genotype) is more often associated with neurological outbreaks, but strains without it also cause myeloencephalopathy.

Who it affects

Practically every horse is infected. Respiratory disease is more common in foals and young horses; abortions affect pregnant mares, sometimes in outbreaks involving several mares on the same farm; myeloencephalopathy is more common in adult and older horses and occurs in outbreaks where many horses gather: competitions, equestrian centres and hospitals.

Anatomy involved

• Brain: vasculitis and thrombosis of small vessels mainly affect the spinal cord, with multifocal lesions in white and grey matter; involvement of the lumbar and sacral segments explains hindquarter weakness and loss of bladder and tail control. The brain, particularly the brainstem, is affected less often.
• Uterus: in the pregnant mare the virus damages the endothelium of the endometrium and of the microcaruncles to which the placenta attaches. Thrombosis separates the placenta from the endometrium and the fetus dies from lack of oxygen; it is expelled fresh, often with the placenta still attached, and almost always without previous signs in the mare. Some fetuses are infected and have lesions in the lung, liver and spleen.
• Trachea: respiratory infection affects the epithelium of the nasal mucosa, pharynx and trachea, from where the virus is shed and enters the blood.

Clinical signs

• Respiratory form: fever, often biphasic, serous nasal discharge and sometimes cough and enlarged mandibular lymph nodes. In adults with immunity it often goes unnoticed.
• Abortion: sudden, in the last third of pregnancy, without previous signs in the mare. Foals infected late in pregnancy can be born alive but weak, with breathing difficulty, and die within a few days.
• Myeloencephalopathy: usually appears a few days after an episode of fever. Sudden-onset ataxia and paresis, more marked in the pelvic limbs, urinary retention or incontinence, loss of tail and anal tone and, in severe cases, recumbency. Signs stabilise within a few days; many horses that stay standing recover, but prolonged recumbency greatly worsens the prognosis.

Diagnosis

• Quantitative PCR on a nasal swab and on whole blood at the same time, to detect nasal shedding and viraemia. In outbreaks, horses without signs should also be sampled.
• Cerebrospinal fluid: increased protein without increased cells (albuminocytological dissociation) and yellow colour (xanthochromia), consistent with vasculitis.
• Abortion: PCR, immunohistochemistry and histopathology of the fetus (lung, liver, spleen, thymus) and placenta.
• Serology is of little help because most horses already have antibodies.
• Myeloencephalopathy outbreaks are notifiable in some countries.

Treatment and prevention

• Supportive treatment: non-steroidal anti-inflammatory drugs, bladder catheterisation, fluid therapy, nursing care and, if needed, a support sling. The use of corticosteroids is debated.
• Antivirals: oral valacyclovir reduces viraemia in experimental studies and is used during outbreaks, including in exposed horses without signs, but evidence that it improves clinical outcome is limited.
• Biosecurity, the most effective measure: isolate horses with fever or signs, take temperatures twice daily in exposed horses, stop movements in and out and maintain quarantine until there are no new cases and PCRs are negative. Pregnant mares should be kept in small, stable groups, apart from horses that travel.
• Vaccines: they reduce virus shedding and respiratory signs, and some are licensed to reduce abortions, with doses in the fifth, seventh and ninth months of pregnancy. None is licensed to prevent myeloencephalopathy, and the protection they give is limited.
• Drug use in horses is subject to each country's regulations and to withdrawal periods. In the EU the horse is a food-producing species, and its identification document (passport) states whether it is excluded from slaughter for human consumption, which determines which drugs may be given.

Key studies

• ACVIM consensus (Lunn et al., 2024): updates the 2009 statement on pathogenesis, strain variation, epidemiology, diagnosis, vaccination, outbreak control and treatment, and is underpinned by 4 systematic reviews. It concludes that evidence that vaccination or treatments work is limited and calls for better-designed studies.
• Osterrieder et al. (2024), systematic review and meta-analysis of 35 vaccine studies (31 experimental) in horses, with GRADE assessment. Sample sizes were small, heterogeneity was large and the quality of evidence was low to moderate for most outcomes (fever, abortion, neurological disease, viraemia, nasal shedding). Commercial and experimental vaccines reduced clinical disease only minimally.
• Goehring et al. (2024), systematic review of pharmacological treatments: of 7,009 studies only 9 met the criteria (valacyclovir, small interfering RNAs, immunomodulators, interferon, heparin and others). Risk of bias was moderate to high and samples were small, and most showed no or minimal benefit. There is no solid evidence that any drug prevents or treats the disease.
• de la Cuesta-Torrado et al. (2025), retrospective study of the outbreak at a show-jumping event in Valencia in 2021, with 191 horses. 73% had clinical signs and 89 developed myeloencephalopathy, of which 12% died (11 of 89). 73% of horses with myeloencephalopathy and 89% of those infected without it returned to competition. Vaccinated horses were more likely to develop myeloencephalopathy (OR 4.54; 95% CI 2.23–9.27), an observational association that does not show the vaccine causes it. The effective reproduction number started at 4.2 and fell below 1 within 2 weeks.
• Goehring et al. (2006), retrospective study of 9 myeloencephalopathy outbreaks in the Netherlands over 4 years, with risk factor analysis in 6. There were 2 to 3 outbreaks per year, with a clear seasonal pattern. Females, older horses and some breeds were at greater risk of severe neurological disease, and it was not seen in horses under 3 years old. These are few outbreaks from a single country.