Equid alphaherpesvirus 1 (EHV-1)

Equid alphaherpesvirus 1 (EHV-1) is a significant viral pathogen in the horse population worldwide, belonging to the Alphaherpesvirinae subfamily (NIH, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7345675/). It is responsible for a variety of clinical manifestations, including respiratory infections (rhinopneumonitis), reproductive failure (abortion), and life-threatening neurological disease known as equine herpesvirus myeloencephalopathy (EHM) (ResearchGate, https://www.researchgate.net/publication/281624353_Equine_herpes_myeloencephalopathy). The virus establishes lifelong latency in the host's nervous and lymphoid tissues, with periodic reactivation leading to shedding and transmission (NIH, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7345675/). Key molecular targets for therapeutic intervention include the viral DNA polymerase (ORF30), which is inhibited by nucleoside analogs like acyclovir and ganciclovir, and the viral thymidine kinase (ORF46), which is essential for the phosphorylation and activation of these prodrugs (Wikipedia, https://en.wikipedia.org/wiki/Thymidine_kinase_from_herpesvirus). EHV-1 entry into host cells is mediated by the interaction of viral glycoprotein D (gD) with the equine major histocompatibility complex class I (MHC-I) receptor (Frontiers, https://www.frontiersin.org/articles/10.3389/fmicb.2020.01342/full). While vaccines exist, they often fail to prevent the neurological form of the disease, leading to a reliance on supportive care and antiviral therapies that aim to reduce viral replication and associated inflammation (Equus Magazine, https://equusmagazine.com/diseases/valacyclovir-ehv1-treatment/).

Other names

Equine herpesvirus 1Equine rhinopneumonitis virusEquid alphaherpesvirus 1

Inhibition of viral DNA polymerase, activation of prodrugs by viral thymidine kinase, inhibition of host JAK/STAT signaling, and inhibition of cyclooxygenase (COX) enzymes.