TOLL LIKE RECEPTOR 3 EXPRESSION PATTERNS IN THE CENTRAL NERVOUS SYSTEM OF BOVINE HERPESVIRUS 5- INFECTED CALVES

MARIN MS; PÉREZ SE; QUINTANA S; LEUNDA MR; PEREYRA SE; MOORE DP; ODEÓN AC

Lima

Congreso; X Congreso de la Asociación Latinoamericana de Inmunología ALAI 2012; 2012

Asociación Latinoamericana de Inmunología ALAI

Bovine herpesvirus 5 (BoHV-5) is the causal agent of necrotizing non-suppurative meningoencephalitis in cattle. In humans, a deficiency of Toll like receptor 3 (TLR3) in the central nervous system (CNS) has been associated with the development ofherpes simplex virusencephalitis. The aim of this study was to determine the relative expression of TLR3 in the CNS of calves infected with BoHV-5 during acute infection, latency and viral reactivation. Twelve calves were inoculated withBoHV-5 at doses of high titer and they were slaughtered during the peak of acute infection. Thirteen calves were inoculated with a low titer doseto induce establishment of latency.Two of them were sacrificed 2 months post-inoculation while the remaining calves were treated with dexamethasone prior to slaughter to stimulate reactivation. Uninfected calves were used as control. Total RNA from several areas of the frontal cortex and trigeminal ganglia of calves was isolated by using Trizol, digested with DNase I and cDNA was synthesized from 1 µg of RNA. Real time RT-PCR was applied  for quantification of TLR mRNA levels. The expression of TRL3 was measured and statistical analysis was performed by using the Relative Expression Software Tool. TLR3 expression was detected in uninfected calves. Up-regulation of TLR3 during acute infection and viral reactivation was observed in some areas of frontal cortex. Statistically significant differences were not detected in TLR3 expression levels in CNS from latently infected calves and in trigeminal ganglia at any stage of infection in neither case. This work is the first report associating TLR3 expression levels to  herpesviral infection in cattle. In-depth descriptions of the protective mechanisms of TLR3 will greatly contribute to its clinical application. Our findings also contribute to the understanding and knowledge of BoHV pathogenesis.