Expression of miR-155 associated with Toll-like receptors 3, 7, and 9 transcription in the olfactory bulbs of cattle naturally infected with BHV5

Abstract

Bovine herpesvirus 5 (BHV5) infection of young cattle is frequently associated with fatal neurological disease and, as such, represents an attractive model for studying the pathogenesis of viral-induced meningoencephalitis. Following replication in the nasal mucosa, BHV5 invades the central nervous system (CNS) mainly through the olfactory pathway. The innate immune response triggered by the host face to virus replication through the olfactory route is poorly understood. Recently, an upregulation of conserved pathogen-associated molecular pattern, as Toll-like receptors (TLRs), has been demonstrated in the CNS of BHV5 experimentally infected cows. A new perspective to understand host-pathogen interactions has emerged elucidating microRNAs (miRNAs) network that interact with innate immune response during neurotropic viral infections. In this study, we demonstrated a link between the expression of TLRs 3, 7, and 9 and miR-155 transcription in the olfactory bulbs (OB) of 16 cows suffering from acute BHV5-induced neurological disease. The OBs were analyzed for viral antigens and genome, miR-155 and TLR 3, 7, and 9 expression considering three major regions: olfactory receptor neurons (ORNs), glomerular layer (GL), and mitral cell layer (ML). BHV5 antigens and viral genomes, corresponding to glycol-C gene, were detected in all OBs regions by fluorescent antibody assay (FA) and PCR, respectively. TLR 3, 7, and 9 transcripts were upregulated in ORNs and ML, yet only ORN layers revealed a positive correlation between TLR3 and miR-155 transcription. In ML, miR-155 correlated positively with all TLRs studied. Herein, our results evidence miR-155 transcription in BHV5 infected OB tissue associated to TLRs expression specifically ORNs which may be a new window for further studies.

Brain-derived neurotrophic factor is down regulated after bovine alpha-herpesvirus 5 infection in both wild-type and TLR3/7/9 deficient mice

“…This is the first study evaluating the effects of BoHV-5 infection in the absence of TLRs 3, 7 and 9 in C57BL/6 mice. There are few works analyzing the role of TLRs during acute bovine herpesvirus-5 infection and those works were restricted to in vitro or in vivo inoculation in cattle so far [33,34,39,43]. Calves infected by intranasal route with 10 6.3 TCID 50 of BoHV-5 showed an increase in the brain expression of TLRs 3, 7, 8 and 9 [34].…”

Immune-related miRNA-mRNA regulation network in the livers of DHAV-3-infected ducklings

“…Meanwhile, the negative miRNA-mRNA network revealed 12 significantly down-regulated miRNAs targeting these TLRs. It has been reported that some miRNAs, like miR-140-5p and welldescribed miR-155, could target TLRs to regulate the innate immune response during the virus infection that had subsequent impact on virus replication [38][39][40]. Upon recognition of pathogens, TLRs recruit a specific set of adaptor molecules, such as MyD88 (myeloid differentiation factor 88) and TIRAP, then initiate downstream signaling events that leads to the secretion of inflammatory cytokines, type I IFN, chemokines, and antimicrobial peptides [41].…”

Exosomal MicroRNA-155 Inhibits Enterovirus A71 Infection by Targeting PICALM

“…Thus, miR-155 affects multiple physiological and pathological functions, including those related to viral infection. Recent studies provided evidence that miR-155 is involved in antiviral innate immunity through Toll-like receptors (TLR3, TLR7, and TLR9) or the nuclear factor kappa-B (NF-кB) signaling pathway [18][19][20]. The innate immune system provides an early phase defense to limit pathogen invasion by recognizing microbial moieties.…”