The Battle between Virus and Host: Modulation of Toll-Like Receptor Signaling Pathways by Virus Infection

Abstract

In order to establish an infection, viruses need to either suppress or escape from host immune defense systems. Recent immunological research has focused on innate immunity as the first line of host defense, especially pattern recognition molecules such as Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), and NOD-like receptors (NLRs). Various microbial components are recognized by their vague and common molecular shapes so-called, pathogen-associated molecular patterns (PAMPs). PAMPs induce inflammatory reactions mediated by the activation of the transcription factor, NF-κB, and by interferons, which lead to an antiviral immune response. Viruses have the capacity to suppress or escape from this pattern recognition molecule-mediated antimicrobial response in various ways. In this paper, we review the various strategies used by viruses to modulate the pattern recognition molecule-mediated innate immune response.

Recognition of pathogen-associated nucleic acids by endosomal nucleic acid-sensing toll-like receptors

“…On the other hand, imbalance between positive and negative regulators of the TLR-associated may disrupt immune homeostasis, resulting in autoimmune diseases. Interestingly, intracellular trafficking of TLR7 and TLR9 from the ER to endosomes is also induced by LPS, which may increase the possibility of autoimmune diseases [186]. Furthermore, autophagy is not only important for the degradation of intracellular pathogens, cellular proteins, and organelles, but also for the regulation of nucleic acid-sensing TLR-mediated recognition of pathogens in multiple ways.…”

“…Thus, a complex network involving multiple regulatory molecules and pathways are likely important for the recognition of endosomal nucleic acid-sensing TLRs, which is essential for preventing serious inflammatory disorders and autoimmune diseases. In addition, nucleic acid-sensing TLR signaling, especially some important adapters such as NF-kB, TRIF, and IRFs, was negatively regulated by viruses (such as VACV, HCV, and HIV and herpesviruses, polyomaviruses, ascoviruses, and adenoviruses), which encoded a number of proteins and miRNAs to inhibit the production of type I IFNs and inflammatory cytokine [186,187].…”

Intracellular Reactive Oxygen Species Production by Polymorphonuclear Leukocytes in Bovine Leukemia Virus-Infected Dairy Cows

“…In fact, IL-10 expression was elevated in the peripheral blood mononuclear cells in PL and AL BLV-infected cattle after three and twelve weeks of experimental infection, respectively [31]. The serum IL-10 level was also enhanced in HTLV-1-infected subjects [32]. In addition, the LPSstimulated macrophages expressing p30 exhibit a marked decrease in the release of pro-inflammatory cytokines and an increase in the release of anti-inflammatory cytokines in HTLV-1 infection [4].…”

“…The role of lymphocytes and monocytes/macrophages in BLV infection has been the subject of many studies in BLVinfected cattle [2,6,8,9,24,31,32], but PMNLs function has been less well investigated [1,7,13,19,29]. Thus, the aim of the present study was to evaluate the function of PMNLs from naturally BLV-infected cows through the evaluation of the intracellular ROS production, even that elicited by Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus).…”

Toll-like receptor 3 (TLR3) and the development of type 1 diabetes mellitus

“…TLR4 activates both pathways, activating NF-kB and inducing type I IFN production. All other TLRs activate exclusively the MyD88-dependent pathway (13,43,44).…”