The Journal of Experimental Medicine
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Published online
doi:10.1084/jem.20062026
The Journal of Experimental Medicine, Vol. 204, No. 6, 1311-1317
The Rockefeller University Press, 0022-1007 $30.00
© Campbell et al.
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BRIEF DEFINITIVE REPORT

 Zoonotic orthopoxviruses encode a high-affinity antagonist of NKG2D

Jessica A. Campbell1, David S. Trossman2, Wayne M. Yokoyama2, and Leonidas N. Carayannopoulos1

1 Division of Pulmonary and Critical Care Medicine and 2 Division of Rheumatology and Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110

CORRESPONDENCE Leonidas N. Carayannopoulos: lcarayan{at}im.wustl.edu

NK and T lymphocytes express both activating and inhibiting receptors for various members of the major histocompatibility complex class I superfamily (MHCISF). To evade immunologic cytotoxicity, many viruses interfere with the function of these receptors, generally by altering the displayed profile of MHCISF proteins on host cells. Using a structurally constrained hidden Markov model, we discovered an orthopoxvirus protein, itself distantly class I–like, that acts as a competitive antagonist of the NKG2D activating receptor. This orthopoxvirus MHC class I–like protein (OMCP) is conserved among cowpox and monkeypox viruses, secreted by infected cells, and bound with high affinity by NKG2D of rodents and humans (KD ~ 30 and 0.2 nM, respectively). OMCP blocks recognition of host-encoded ligands and inhibits NKG2D-dependent killing by NK cells. This finding represents a novel mechanism for viral interference with NKG2D and sheds light on intercellular recognition events underlying innate immunity against emerging orthopoxviruses.


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