Toll-like receptor expression in the nervous system of bovine alpha-herpesvirus-infected calves.

MARIN, M; QUINTANA, S; LEUNDA, M; ODEÓN, A; PEREZ, S. E

Mar del Plata

Jornada; LIX Reunión Científica anual de la Sociedad Argentina de Investigación Clínica (SAIC), LXII Reunión Anual de la Sociedad Argentina de Inmunología (SAI); 2014

Sociedad Argentina de Inmunología (SAI).

Alpha-herpesviruses are capable of causing neurologic disease in cattle. In this study, the expression levels of viral Toll-like receptors (TLRs) in the nervous system of bovine herpesvirus 5 (BoHV-5)-infected calves were investigated. Twelve calves were inoculated with BoHV-5 at doses of high titer (106.3 TCID50) and they were slaughtered during the peak of acute infection. Thirteen calves were challenged with a low virus titer (103 TCID50) to induce the establishment of latency. Two of them were euthanized 2 months post-inoculation while the remaining calves were treated with dexamethasone to stimulate reactivation. Uninfected calves were used as control and BoHV-1-infected calves were used to determine whether TLR signalling had influence on the differences on neuropathogenicity between both alpha-herpesviruses. Total RNA from several areas of the frontal cortex and trigeminal ganglia of calves was isolated by using Trizol and Real time RT-PCR was applied for quantification of TLRs 3 and 7-9 mRNA levels. Statistical analysis was performed by using the Relative Expression Software Tool. A significant increase in the expression of TLRs 3 and 7-9 was found in the anterior cerebral cortex during acute infection and BoHV-5 reactivation. In the trigeminal ganglia, only TLR9 expression was significantly affected by infection. The magnitude of the increase was lower in BoHV-1-infected calves, suggesting that a restricted immune response might protect against exacerbated inflammatory responses in the brain. This work describes, for the first time, the involvement of TLRs 3 and 7-9 in the recognition of BoHV in the bovine nervous system, indicating that the expression of these receptors might be associated with the development of neurological disease. Modulation of the signalling pathways mediated by TLRs might provide an effective approach to control the neuro-immune response to BoHV-5, which may, in part, be responsible the neurological lesions caused by the virus.