Abstract
Respiratory syncytial virus (RSV) is the leading cause of severe acute lower respiratory tract infections in infants worldwide. Although several pattern recognition receptors (PRRs) can sense RSV-derived pathogen-associated molecular patterns (PAMPs), infection with RSV is typically associated with low to undetectable levels of type I interferons (IFNs). Multiple RSV proteins can hinder the host’s innate immune response. The main players are NS1 and NS2 which suppress type I IFN production and signalling in multiple ways. The recruitment of innate immune cells and the production of several cytokines are reduced by RSV G. Next, RSV N can sequester immunostimulatory proteins to inclusion bodies (IBs). N might also facilitate the assembly of a multiprotein complex that is responsible for the negative regulation of innate immune pathways. Furthermore, RSV M modulates the host’s innate immune response. The nuclear accumulation of RSV M has been linked to an impaired host gene transcription, in particular for nuclear-encoded mitochondrial proteins. In addition, RSV M might also directly target mitochondrial proteins which results in a reduced mitochondrion-mediated innate immune recognition of RSV. Lastly, RSV SH might prolong the viral replication in infected cells and influence cytokine production.
Highlights
Human respiratory syncytial virus (RSV) is an enveloped, negative-stranded RNA virus that is classified in the Pneumoviridae family of the order Mononegavirales
pattern recognition receptors (PRRs) are crucial for the recognition of molecules that are present in pathogens, the socalled pathogen-associated molecular patterns (PAMPs) [12]
These results suggest that A20 requires at least two other proteins (TAX1BP1 and A20-binding inhibitor of NF-κB1 (ABIN1)) to interrupt the innate immune response in RSV-infected epithelial cells
Summary
Human respiratory syncytial virus (RSV) is an enveloped, negative-stranded RNA virus that is classified in the Pneumoviridae family of the order Mononegavirales. RSV is the leading cause of severe acute lower respiratory tract infections (ALRI) in infants worldwide [1]. There were approximately 500,000 hospital admissions of older adults due to RSV-associated acute respiratory infection in 2015 [3]. In response to virus infection, many elements of the host’s innate immune system are deployed as an early line of defense [5,6]. Activated PRRs trigger several signaling pathways that eventually lead to an upregulated interferon (IFN) gene expression. The quality of the innate immune response is a major determinant for RSV disease severity [9]. RSV has evolved several mechanisms to circumvent the host’s innate immunity in order to promote virus replication. We highlight and discuss the mechanisms exploited by the different RSV proteins in innate immune evasion
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