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How RSV Proteins Join Forces to Overcome the Host Innate Immune Response
| Content Provider | MDPI |
|---|---|
| Author | Royen, Tessa Van Rossey, Iebe Sedeyn, Koen Schepens, Bert Saelens, Xavier |
| Copyright Year | 2022 |
| Description | 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. |
| Starting Page | 419 |
| e-ISSN | 19994915 |
| DOI | 10.3390/v14020419 |
| Journal | Viruses |
| Issue Number | 2 |
| Volume Number | 14 |
| Language | English |
| Publisher | MDPI |
| Publisher Date | 2022-02-17 |
| Access Restriction | Open |
| Subject Keyword | Viruses Infectious Diseases Respiratory Syncytial Virus Innate Immunity Interferon Non-structural Proteins |
| Content Type | Text |
| Resource Type | Article |