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Journal of Biomedicine and Biotechnology
Volume 2011 (2011), Article ID 724607, 12 pages
Review Article

How the Virus Outsmarts the Host: Function and Structure of Cytomegalovirus MHC-I-Like Molecules in the Evasion of Natural Killer Cell Surveillance

1Molecular Biology Section, Laboratory of Immunology, NIAID, National Institutes of Health, Bethesda, MD 20892-1892, USA
2Department of Virology, University of the Witwatersrand, Johannesburg 2050, South Africa
3Department of Medical Virology, University of Pretoria, Pretoria 0001, South Africa

Received 25 February 2011; Accepted 28 March 2011

Academic Editor: John E. Coligan

Copyright © 2011 Maria Jamela Revilleza et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Natural killer (NK) cells provide an initial host immune response to infection by many viral pathogens. Consequently, the viruses have evolved mechanisms to attenuate the host response, leading to improved viral fitness. One mechanism employed by members of the β-herpesvirus family, which includes the cytomegaloviruses, is to modulate the expression of cell surface ligands recognized by NK cell activation molecules. A novel set of cytomegalovirus (CMV) genes, exemplified by the mouse m145 family, encode molecules that have structural and functional features similar to those of host major histocompatibility-encoded (MHC) class I molecules, some of which are known to contribute to immune evasion. In this review, we explore the function, structure, and evolution of MHC-I-like molecules of the CMVs and speculate on the dynamic development of novel immunoevasive functions based on the MHC-I protein fold.