Activation of toll-like receptor signaling pathways leading to nitric oxide-mediated antiviral responses
| Autor: | Mohamed Faizal Abdul-Careem, Aruna Amarasinghe, Mohamed Sarjoon Abdul-Cader |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Review Infectious Bursal Disease Virus Nitric Oxide Nitric oxide 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Immune system Downregulation and upregulation Virology Animals Humans RNA Viruses Receptor Influenza Virus Infection Toll-like receptor biology Toll-Like Receptors DNA Viruses Signal transducing adaptor protein General Medicine Cell biology Nitric oxide synthase 030104 developmental biology chemistry Virus Diseases 030220 oncology & carcinogenesis biology.protein Respiratory Syncytial Virus Antiviral Mechanism Signal transduction Signal Transduction |
| Zdroj: | Archives of Virology |
| ISSN: | 1432-8798 0304-8608 |
| Popis: | Toll-like receptors (TLRs), well-characterized pattern-recognizing receptors of the innate arm of the immune system, are vital in detecting pathogen-associated molecular patterns (PAMPs). The TLR-PAMP interaction initiates an intracellular signaling cascade, predominantly culminating in upregulation of antiviral components, including inducible nitric oxide synthase (iNOS). After activation, various TLR pathways can promote iNOS production via the myeloid differentiation primary response-88 (MyD-88) adapter protein. Subsequently, iNOS facilitates production of nitric oxide (NO), a highly reactive and potent antiviral molecule that can inhibit replication of RNA and DNA viruses. Furthermore, NO can diffuse freely across cell membranes and elicit antiviral mechanisms in various ways, including direct and indirect damage to viral genomes. This review emphasizes current knowledge of NO-mediated antiviral responses elicited after activation of TLR signaling pathways. |
| Databáze: | OpenAIRE |
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