RSV Activates Innate Immunity through Toll-like Receptor 2

UMMS Affiliation

Graduate School of Biomedical Sciences; Department of Medicine

Publication Date


Document Type



Life Sciences | Medicine and Health Sciences


Respiratory Syncytial Virus (RSV) is a common infection that is associated with a range of respiratory illnesses from common cold-like symptoms to serious lower respiratory tract illnesses such as pneumonia and bronchiolitis. RSV is the single most important cause of serious lower respiratory tract illness in children < 1 year of age. Host innate and acquired immune responses activated following RSV infection have been suspected as contributing to RSV disease. Toll-like Receptors (TLRs) activate innate and acquired immunity and are candidates for playing key roles in the host immune response to RSV. Leukocytes express TLRs including TLR2, TLR6, TLR3, TLR4, and TLR7 that can potentially interact with RSV and promote immune responses following infection. Using knock out mice we have demonstrated TLR2 and TLR6 signaling in leukocytes can activate innate immunity against RSV by promoting TNF-alpha, IL-6, CCL2 (MCP-1), and CCL5 (RANTES). As previously noted, TLR4 also contributed to cytokine activation. Furthermore, we demonstrated that signals generated following TLR2 and TLR6 activation were important for controlling viral replication in vivo. Additionally TLR2 interactions with RSV promoted neutrophil migration and dendritic cell activation within the lung. Collectively, these studies indicate TLR2 is involved in RSV recognition and subsequent innate immune activation.

DOI of Published Version



J Virol. 2008 Nov 19. Link to article on publisher's site

Journal/Book/Conference Title

Journal of virology

Related Resources

Link to Article in PubMed

PubMed ID