Equine herpesvirus type 1 induces both neurological and respiratory disease in Syrian hamsters

Evaluation of Viral Migration of Different Variants of Equid Alphaherpesvirus 1 in the Central Nervous System of Hamsters by Immunohistochemistry

“…As reported by other authors, we also found variation in severity of clinical signs, according the pathogenicity of the virus variant [15,30]. Variants A9/92 and A4/72 showed high neurovirulence, compared to the other tested variants, with results similar to those reported in mice after intranasal inoculation [18]; the Iso72/10 variant showed lighter neurological signs with acute phase starting only at 4 dpi and presented also respiratory signs while A3/97 and AR4 variants caused predominantly respiratory signs [32]. In a study using several line ages of mice, the A3/97 variant caused no weight loss or apparent clinical signs of disease, although it was possible to recover the virus from lung of all infected mice and from brain of a single BALBc nude mouse [18].…”

“…The microscopic lesions were similar to those reported in hamsters infected with EHV-9 and in mice and hamsters inoculated with EHV-1, with the olfactory bulb and frontal cortex being the primary affected regions after intranasal inoculation [8,16,28,29,31,32]. In hamster and murine models, the intranasally inoculated virus migrates from the nasal mucosa by neural dissemination via the olfactory neuroepithelium throughout the olfactory bulb, olfactory nerve, and ventricular surface, leading to neuronal degeneration, mainly in cortical areas and the hippocampus, with associated generalized ventriculitis [16,18,28,30].…”

“…Hamsters infected with Iso/72, A3/97 and AR4 presented CNS lesions predominantly inflammatory (meningo-encephalitis) while hamsters inoculated with A4/72 and A9/92 showed predominantly neuronal necrosis with vacuolization of the neuroparenchyma, perineuronal and perivascular edema, with liquefactive necrosis in many areas of the CNS instead of inflammatory changes [32].…”

“…In adult horses, EHM induces microvascular damage to the central nervous system via initiation of an inflammatory cascade followed by degenerative thrombotic vasculitis of small blood vessels in the brain or spinal cord with resultant ischemic neuronal necrosis, perivascular mononuclear cuffing, congestion, hemorrhage, diffuse gliosis, perineuronal and perivascular edema [7,12,44]. In hamsters is suggested that these lesions may be the result of the viral replication within neurons, as opposed to vascular changes [32].…”

“…In subsequent years, the model of EHV-1 infection in hamster was used for the study of antiviral agents [25] and immune response to the virus [26,27]. Recently, hamster models have been used to study the neuropathogenesis of EHV-9 [28][29][30][31], but there are few studies about neuropathogenicity of EHV-1 in hamster models [32].…”