Role of MyD88 in route-dependent susceptibility to vesicular stomatitis virus infection
Authors
Zhou, ShenghuaKurt-Jones, Evelyn A.
Fitzgerald, Katherine A.
Wang, Jennifer P.
Cerny, Anna M.
Chan, Melvin
Finberg, Robert W.
UMass Chan Affiliations
Department of Medicine, Division of Infectious Diseases and ImmunologyDocument Type
Journal ArticlePublication Date
2007-04-04Keywords
AnimalsAntibodies, Viral
CD4-Positive T-Lymphocytes
Chemokine CCL2
Disease Susceptibility
Interferon Type II
Interferon-alpha
Interleukin-1
Lymphocyte Activation
Mice
Mice, Inbred C57BL
Mice, Knockout
Myeloid Differentiation Factor 88
Rhabdoviridae Infections
*Vesicular stomatitis Indiana virus
Immunology and Infectious Disease
Life Sciences
Medicine and Health Sciences
Metadata
Show full item recordAbstract
TLRs are important components of the innate immune response. The role of the TLR signaling pathway in host defense against a natural viral infection has been largely unexplored. We found that mice lacking MyD88, an essential adaptor protein in TLR signaling pathway, were extremely sensitive to intranasal infection with vesicular stomatitis virus, and this susceptibility was dose dependent. We demonstrated that this increased susceptibility correlates with the impaired production of IFN-alpha and defective induction and maintenance of neutralizing Ab. These studies outline the important role of the TLR signaling pathway in nasal mucosae-respiratory tracts-neuroepithelium environment in the protection against microbial pathogen infections. We believe that these results explain how the route of infection, probably by virtue of activating different cell populations, can lead to entirely different outcomes of infection based on the underlying genetics of the host.Source
J Immunol. 2007 Apr 15;178(8):5173-81.
DOI
10.4049/jimmunol.178.8.5173Permanent Link to this Item
http://hdl.handle.net/20.500.14038/38426PubMed ID
17404300Related Resources
ae974a485f413a2113503eed53cd6c53
10.4049/jimmunol.178.8.5173