The mouse model was used to study the pathogenesis of equine herpesvirus type 1 (EHV-1) after primary and secondary intranasal infections. This review examines the similarities and differences in the pathogenesis of primary EHV-1 infection in the natural host, the horse, and in the mouse by comparing tissue tropism, clinical signs of infection, the effects of EHV-1 on pregnancy, haematological changes following infection, viral clearance, histopathology and latency. Next to the lung, EHV-1 was transmitted early and directly to the brain, both via the olfactory route and the trigeminal nerve, but traces of degenerative or inflammatory processes were not detected there. In addition, replication of the IR4 mutant was abrogated in all other cell types tested, including equine ETCC tumor cells and cells of mouse, rabbit, monkey, and human origin. Successful infection was clinically apparent as each of the foals had febrile responses, nasal discharge, and enlarged submandibular lymph nodes. Both humoral and cell-mediated responses to the infection were detected and monitored. Viruses often integrate in their own genomes several cellular genes involved in the control of cell growth and differentiation and/or in the regulation of immune functions.
Intranasal infection of EHV-4 on serologically negative local yearling ponies results in a disease characterised by clinical signs of nasal discharge and fever.