Journal
CELL DEATH AND DIFFERENTIATION
Volume 10, Issue 12, Pages 1320-1328Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.cdd.4401308
Keywords
herpes simplex virus; Us3 protein kinase; granzyme B; cytotoxic T cells; apoptosis; B lymphoblasts
Categories
Ask authors/readers for more resources
The Us3 kinase is part of the antiapoptotic arsenal that salvages herpes simplex virus (HSV)-1-infected cells from damage caused by different stimuli. We demonstrate that Us3 protects HSV-1-infected cells from lysis by MHC class I-restricted CD8T cells without affecting antigen presentation. Expression of Us3 was associated with inhibition of caspase activation and reduced cleavage of the proapoptotic protein Bid. Recombinant granzyme B (GrB) failed to cleave Bid in cytosolic extracts from Us3 positive cells, while recombinant Bid served as substrate for Us3 phosphorylation, suggesting that modification of Bid by Us3 blocks its processing by GrB. Our data illustrate a new strategy of viral escape, where modification of a cellular proapoptotic substrate may prevent lysis of the infected cells without affecting other T-cell functions.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available