期刊
CELLULAR MICROBIOLOGY
卷 12, 期 2, 页码 148-157出版社
WILEY
DOI: 10.1111/j.1462-5822.2009.01385.x
关键词
-
资金
- NIH, (Northeast Biodefense Center-Lipkin) [U54 AI057158]
- NIH [AI059536]
Cathepsins B and L contribute to Ebola virus (EBOV) entry into Vero cells and mouse embryonic fibroblasts. However, the role of cathepsins in EBOV-infection of human dendritic cells (DCs), important targets of infection in vivo, remains undefined. Here, EBOV-like particles containing a beta-lactamase-VP40 fusion reporter and Ebola virus were used to demonstrate the cathepsin dependence of EBOV entry into human monocyte-derived DCs. However, while DC infection is blocked by cathepsin B inhibitor, it is insensitive to cathepsin L inhibitor. Furthermore, DCs pre-treated for 48 h with TNF alpha were generally less susceptible to entry and infection by EBOV. This decrease in infection was associated with a decrease in cathepsin B activity. Thus, cathepsin L plays a minimal, if any, role in EBOV infection in human DCs. The inflammatory cytokine TNF alpha modulates cathepsin B activity and affects EBOV entry into and infection of human DCs.
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