Abstract
Interferons are a group of small proteins that play key roles in host antiviral innate immunity. Their induction mainly relies on host pattern recognition receptors (PRR). Host PRR for RNA viruses include Toll-like receptors (TLR) and retinoic acid-inducible gene I (RIG-I) like receptors (RLR). Activation of both TLR and RLR pathways can eventually lead to the secretion of type I IFNs, which can modulate both innate and adaptive immune responses against viral pathogens. Because of the important roles of interferons, viruses have evolved multiple strategies to evade host TLR and RLR mediated signaling. This review focuses on the mechanisms of interferon induction and antagonism of the antiviral strategy by RNA viruses.
Highlights
Host immunity can be divided into two broad categories: innate and adaptive
These discoveries led to the identification of a conserved signaling pathway of the immune response: the Drosophila Toll-Dorsal pathway, which is considered the homologue of the interleukin-1 receptor (IL-1R)-NF-κB pathway in mammals [23]
It has been shown that TLR10 plays a role in mediating bacterial peptidoglycan-induced trophoblast apoptosis, which implies that TLR10 may recognize a bacteria-derived component [67]
Summary
Host immunity can be divided into two broad categories: innate and adaptive. Innate immunity is known as non-specific resistance against infection, while adaptive immunity indicates acquired immune responses that are specific against invading pathogens. The innate immunity consists of physical, cellular and chemical components. Interferons are a major player in the chemical components of innate immunity against viral infection. Since the discovery of interferon in the. Along with the development of molecular biology, many genes encoding the interferons have been cloned and sequenced, as well as expressed in prokaryotic system. With the availability of purified interferons, interferon-based therapy has been developed and applied to treat cancer and viral infection. Interferons, their classification and functions, induction pathways leading to their production, and virus-mediated antagonism will be described
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