Study: Neurologic Strain of Equine Herpesvirus-1 Increasing

The number of equine herpesvirus type-1 (EHV-1) infections caused by the neuropathogenic form of the virus has been steadily increasing over the past 51 years, report researchers from the University of Kentucky.

Clinical observations suggest that neuropathogenic strains of EHV-1 (i.e., strains of EHV-1 with a single mutation in the gene that encodes the enzyme called DNA polymerase) have become more prevalent. These infections result in significant economic losses for equine industries worldwide.

To see if there was any truth to this apparent trend, Udeni B. R. Balasuriya, BVSc, MS, PhD, an associate professor of virology at the Gluck Equine Research Center in Lexington, Ky., and colleagues analyzed 426 archived isolates of EHV-1 collected from aborted equine fetuses between 1951 and 2006.

They found that not only is the neuropathogenic strain of the virus becoming increasingly common, but that it really isn’t all that new. Even some of the EHV-1 isolates collected from fetuses aborted in the 1950s were the neuropathogenic strain.

According to the study, 38 (8.9%) of the 426 isolates were the neuropathogenic strain.

In the article, the authors relayed that the prevalence of EHV-1 isolates containing the mutation increased from 3.3% in the 1960s, 7.7% in the 1970s, 5.8% in the 1980s, to 14.4% in the 1990s. Further, 19.4% of the viral samples from 2000 to 2006 had the neuropathogenic genotype.

One additional noteworthy finding reported in this study was the identification of additional genetic mutations in the nearby genome of two of the archived EHV-1 isolates. Research regarding additional mutations is ongoing.

The study, "The increased prevalence of neuropathogenic strains of EHV-1 in equine abortions," is scheduled to be published in an upcoming edition of the journal Veterinary Microbiology. The abstract is available on PubMed.  

Disclaimer: Seek the advice of a qualified veterinarian before proceeding with any diagnosis, treatment, or therapy.