1. Respiratory syncytial virus (RSV) infection and the host.
Respiratory syncytial virus (RSV) infection and the host. The innate and adaptive immune response to RSV. a) Viral RNA, arising during viral replication, is recognised through Toll-like receptor (TLR)-3 and retinoic acid-inducible gene (RIG)-I-like receptors. Cellular infection triggers the release of early inflammatory mediators (e.g. interferons (IFNs) and tumour necrosis factor (TNF)-α) and chemokines (e.g. CXCL8 and CXCL11). Type I IFNs upregulate pro-apoptotic factors in the epithelial cells, while TNF-α and chemokines recruit natural killer (NK) cells and polymorphonuclear leukocytes (PMNs) that have the ability to kill the infected cells, thus limiting viral replication and spread to neighbouring cells in the first days of infection. b) RSV can also infect dendritic cells that carry viral antigens to regional lymph nodes. Presentation of viral antigens to CD4+ T-lymphocytes occurs and primed T-cells activate B-lymphocytes and CD8+ T-cells. They all migrate back to the infected epithelium with further release of mediators and recruitment of additional inflammatory cells, including PMNs and mononuclear cells. Data from [39].
Giovanni A. Rossi, and Andrew A. Colin Eur Respir J 2015;45:
©2015 by European Respiratory Society