Equid herpesvirus 1 is neurotropic in mice, but latency from which infectious virus can be reactivated does not occur

Abstract

Equid herpesvirus 1 (EHV-1) is the most common cause of virus-induced abortion in horses. After primary infection the virus becomes latent predominantly in the respiratory tract lymph nodes and the genome can also be detected in the peripheral nervous system. The role of mouse as a feasible model for the establishment of latency and reactivation of EHV-1 was investigated. Intracerebral and intranasal infections of 3-and 17-day-old mice were made and virus replication was confirmed by virus isolation and detected by indirect immunofluorescence (IIF) in brain. For reactivation studies, the mice were killed 8 weeks post infection and tissues were collected for cocultivation. In mice from both age groups, infectious virus was not detected by cocultivation. Following attempts to reactivate virus in vivo with corticosteroids, the viral antigen was detected at low levels by IIF and the expression of the gB gene by reverse transcription polymerase chain reaction (RT-PCR) in brain, trigeminal ganglia, olfactory lobe, lung and spleen. Virus was also detected by IIF following incubation of tissue explants in the growth medium containing pokeweed mitogen (PWM). These results show the limitations of the mouse model for investigating EHV-1 latency and highlights the issue of 'ineffective reactivation' of virus.

Pathogenesis of equine herpesvirus‐1 infection in the mouse model

“…In one study, EHV‐1 antigen was demonstrated by indirect immunofluorescence in the trigeminal ganglia of adult mice 2 months after i.n. inoculation (40). Such scattered observations presenting virus in the trigeminal ganglia might be explained by the slight traumatization of the nasal mucosa during the instillation procedure.…”