Abstract
Herpesviruses are known for their persistent lifelong latent infection, which is made possible by their vast repertoire of immune-evasion strategies. We have previously shown that a human cytomegalovirus (HCMV) microRNA represses expression of the stress-induced Natural Killer (NK) cell ligand, MICB, to escape recognition and consequent elimination by NK cells. Here, we show functional conservation among diverse microRNAs derived from different herpesviruses, including HCMV, Kaposi's sarcoma-associated herpesvirus (KSHV), and Epstein-Barr virus (EBV), in their ability to directly target MICB mRNA and reduce its expression. Although the various viral microRNAs share no sequence homology, they are functionally similar and target MICB at different yet adjacent sites during authentic viral infection. The finding that different herpesvirus microRNAs target MICB indicates that MICB plays a pivotal role in the clash between herpesviruses and humans.
Original language | English |
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Pages (from-to) | 376-385 |
Number of pages | 10 |
Journal | Cell Host and Microbe |
Volume | 5 |
Issue number | 4 |
DOIs | |
State | Published - 23 Apr 2009 |
Bibliographical note
Funding Information:This study was supported by grants from the U.S.-Israel Binational Science Foundation, the Israeli Cancer Research Foundation, the Israeli Science Foundation, the European Consortium (MRTN-CT-2005 and LSCH-CT-2005-518178), and the Association for International Cancer Research, all to O.M. O.M. is a Crown Professor of Molecular Immunology.
Keywords
- MICROBIO
- MOLIMMUNO
- RNA