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Type 1 interferon (IFN) receptor gene knockout (IFNAR−/−) mouse embryo fibroblasts (MEFs) are more susceptible to and productive of West Nile virus (WNV) and produce less type 1 IFN than WNV-infected wildtype (wt) MEFs. WNV infection of IFNAR−/− MEFs induced activation of a p65/p50 heterodimer of nuclear factor (NF)-κB and up-regulation of cell-surface expression of major histocompatibility complex class I (MHCI) molecules. WNV infection of wt MEFs resulted in a greater up-regulation of MHC-I than did infection of IFNAR−/− MEFs because of the action of endogenous type 1 IFN production. IFN-β-treatment of wt MEFs did not activate NF-κB but did up-regulate cell-surface MHC-I expression. The WNV-induced NF-κB activation was partially abrogated by the serine protease inhibitor N-benzoyl-l-tosyl-l-phenylalanine, which also abrogated the up-regulation of MHC-I. Thus, we demonstrate 2 pathways for WNV-induced up-regulation of MHCI, a WNV-induced NF-κB-dependent, IFN-independent pathway and an NF-κB-independent, IFN-dependent pathway.

© 2004 by the Infectious Diseases Society of America
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Major Articles, Brief Reports, and Perspective > Viruses > Major Articles
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