Inflammasomes and its importance in viral infections

Abstract

A complex interplay between pathogen and host determines the immune response during viral infection. A set of cytosolic sensors are expressed by immune cells to detect viral infection. NOD-like receptors (NLRs) comprise a large family of intracellular pattern recognition receptors. Members of the NLR family assemble into large multiprotein complexes, termed inflammasomes, which induce downstream immune responses to specific pathogens, environmental stimuli, and host cell damage. Inflammasomes are composed of cytoplasmic sensor molecules such as NLRP3 or absent in melanoma 2 (AIM2), the adaptor protein ASC (apoptosis-associated speck-like protein containing caspase recruitment domain), and the effector protein procaspase-1. The inflammasome operates as a platform for caspase-1 activation, resulting in caspase-1-dependent proteolytic maturation and secretion of interleukin (IL)-1b and IL-18. This, in turn, activates the expression of other immune genes and facilitates lymphocyte recruitment to the site of primary infection, thereby controlling invading pathogens. Moreover, inflammasomes counter viral replication and remove infected immune cells through an inflammatory cell death, program termed as pyroptosis. As a countermeasure, viral pathogens have evolved virulence factors to antagonise inflammasome pathways. In this review, we discuss the role of inflammasomes in sensing viral infection as well as the evasion strategies that viruses have developed to evade inflammasome-dependent immune responses. This information summarises our understanding of host defence mechanisms against viruses and highlights research areas that can provide new approaches to interfere in the pathogenesis of viral diseases.

Transmissible gastroenteritis virus infection induces NF-κB activation through RLR-mediated signaling

“…The priming step to activate the production of inflammatory cytokines is mediated primarily by TLRs and/or RLRs signaling (Shrivastava et al, 2016). To determine which signaling pathway is triggered by TGEV to activate NF-κB, specific siRNAs targeting MyD88, TRIF, MAVS, and STING, adaptor molecules in the TLR and RLR pathways, were synthesized.…”

“…Virus invasion always triggers an inflammatory response, which is a key mediator of the host response against microbial pathogens (Shrivastava et al, 2016). To monitor and rapidly respond to diverse viruses, germline-encoded pattern recognition receptors (PRRs) are appointed to sense pathogen-associated molecular patterns (PAMPs) and subsequently induce the production of inflammatory mediators with a two-step process: priming and activation (Poeck and Ruland, 2012;Rietdijk et al, 2008).…”

A STING to inflammation and autoimmunity

“…TLRs play a vital role in the pathogenesis of autoimmunity through the failure of the mechanism of self‐recognition . Inflammasomes are another class of intracellularly expressed PRRs recognizing intracellular PAMPs and DAMPs . The inflammasome‐mediated recognition of cytosolic PAMPs and DAMPs promotes necroptosis and the release of IL‐1β and IL‐18 .…”

Immunity to Avian Leukosis Virus: Where Are We Now and What Should We Do?

“…Caspase-1 expression combined with adaptor NLRP3 enabled IL-1β and IL-18 increases at 5 or 7 dpi (30). NLRP3 is an important initiator protein of the inflammasome, a multicomponent complex that activates caspase-1 and results in IL-1β and IL-18 secretion (31). However, this is the extent of this type of data but indicates that further research would yield fruitful results.…”