Diverse Herpesvirus MicroRNAs Target the Stress-Induced Immune Ligand MICB to Escape Recognition by Natural Killer Cells

Daphna Nachmani, Noam Stern-Ginossar, Ronit Sarid, Ofer Mandelboim*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

399 Scopus citations

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 languageAmerican English
Pages (from-to)376-385
Number of pages10
JournalCell Host and Microbe
Volume5
Issue number4
DOIs
StatePublished - 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

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