Primary Infection, Latency, and Reactivation of Bovine Herpesvirus Type 5 in the Bovine Nervous System

Abstract

Abstract. Bovine herpesvirus type 5 (BHV-5) infection in calves causes meningoencephalitis, a fatal disease highly prevalent in South America. To study the pathogenesis of BHV-5 infection in cattle, 12 calves (group 1: acute infection) and 11 calves (group 2: latent infection) were intranasally inoculated with an Argentinean BHV-5 isolate at 10 8 and 10 4.7 tissue culture infective doses, respectively; six calves (control group) were mock infected. At 3 months postinoculation, all of the calves in group 2 and three calves in group 3 were given dexamethasone to reactivate the virus. The animals were euthanatized between days 6 and 17 postinoculation (group 1) and between days 6 and 16 postreactivation (group 2). Seventy-five percent and 91% of animals in groups 1 and 2, respectively, excreted BHV-5 in nasal and ocular discharges. Following dexamethasone administration, 45% of calves shed virus in both types of secretions. Spontaneous virus reactivation and shedding was observed in one calf. Neurologic signs consisting of circling, teeth grinding, ptyalism, jaw chomping, tongue protrusion, and apathy were observed in two animals in group 1 and, during the reactivation period, in four animals in group 2. Macroscopic findings consisted of softening of the cerebral tissue, meningeal hemorrhages and swelling, and edema and hemorrhages of prescapular, retropharyngeal and submandibular lymph nodes. Histologic lesions consisted of meningitis, mononuclear perivascular cuffing, neuronophagia, satellitosis, gliosis, hemorrhage, and necrosis and edema. Lesions in anterior cerebral cortex, medulla, and pons were consistently seen in all the animals of group 1. In the acutely infected animals, lesions in the diencephalon appeared at day 10 postinoculation, whereas in the latently infected calves these lesions were observed as early as at day 6 postreactivation. Latently infected animals developed lesions simultaneously in anterior cortex, medulla, pons, and diencephalon, showing a remarkable difference from the acutely infected group. Trigeminal ganglionitis appeared relatively early in animals of both groups (day 7 postinoculation in group 1 and day 8 postreactivation in group 2).

Ruminant alphaherpesviruses related to bovine herpesvirus 1

“…In the next phase, calves are affected by muscle trembling, circling to one side, pushing their head against a wall and ataxia, followed by seizure-like episodes and opisthotonos [83]. Histological lesions in the brain consist of meningitis, mononuclear perivascular cuffing, neurophagia, satellitosis, gliosis, haemorrhage, necrosis and oedema [92].…”

Reativação e distribuição do DNA latente do herpesvírus bovino tipo 5 no encéfalo de ovinos infectados experimentalmente

“…Em alguns animais, a invasão do encéfalo é restrita e o vírus estabelece infecção latente nos gânglios trigêmeos (TG) e em outros sítios do SNC (Perez et al 2002, Vogel et al 2003. A infecção latente pode ser reativada naturalmente ou pode ser induzida pela administração de corticoides (Perez et al 2002, Vogel et al 2003.…”

Production and characterization of monoclonal antibodies to a Brazilian bovine herpesvirus type 5

“…Outbreaks of neurological disease induced by BHV-5 have been frequently described in well-defined geographical regions, mainly Argentina and central/southern Brazil (2)(3)(4). Clinical signs of BHV-5-associated neurological disease include tremors, circling, bruxism, incoordination, nystagmus, recumbency followed by I. Oldoni et al convulsions, paddling, and inevitably death (2,4,5). Like other α-herpesviruses, BHV-5 establishes a lifelong latent infection in sensory nerve ganglia after primary infection (5,6).…”

“…Clinical signs of BHV-5-associated neurological disease include tremors, circling, bruxism, incoordination, nystagmus, recumbency followed by I. Oldoni et al convulsions, paddling, and inevitably death (2,4,5). Like other α-herpesviruses, BHV-5 establishes a lifelong latent infection in sensory nerve ganglia after primary infection (5,6). Viral reactivation and shedding may occur under certain induced or naturally occurring stimuli and provide favorable conditions for viral transmission and spread (5,7).…”

“…Like other α-herpesviruses, BHV-5 establishes a lifelong latent infection in sensory nerve ganglia after primary infection (5,6). Viral reactivation and shedding may occur under certain induced or naturally occurring stimuli and provide favorable conditions for viral transmission and spread (5,7).…”