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Journal of Virology, March 2005, p. 2920-2930, Vol. 79, No. 5
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.5.2920-2930.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Selective Down-Regulation of the NKG2D Ligand H60 by Mouse Cytomegalovirus m155 Glycoprotein

Milena Hasan,1 Astrid Krmpotic,1 Zsolt Ruzsics,2 Ivan Bubic,1 Tihana Lenac,1 Anne Halenius,3 Andrea Loewendorf,4 Martin Messerle,4 Hartmut Hengel,3,{dagger} Stipan Jonjic,1* and Ulrich H. Koszinowski2

Department of Histology and Embryology, Faculty of Medicine, University of Rijeka, Rijeka, Croatia,1 Max von Pettenkofer Institute, Ludwig Maximilians University of Munich, Munich,2 Division of Viral Infections, Robert Koch-Institute, Berlin,3 Virus Cell Interaction Group, ZAMED, Medical Faculty, Martin Luther University of Halle-Wittenberg, Halle (Saale), Germany4

Received 7 May 2004/ Accepted 8 October 2004

Both human and mouse cytomegaloviruses (CMVs) encode proteins that inhibit the activation of NK cells by down-regulating cellular ligands for the activating NK cell receptor NKG2D. Up to now, three ligands for the NKG2D receptor, named RAE-1, H60, and MULT-1, have been identified in mice. The resistance of mouse strains to murine CMV (MCMV) infection is determined by their ability to generate an effective NK cell response. The MCMV gene m152, a member of the m145 gene family, down-regulates the expression of RAE-1 in order to avoid NK cell control in vivo. Here we report that the m155 gene, another member of the m145 gene family, encodes a protein that interferes with the expression of H60 on the surfaces of infected cells. Deletion of the m155 gene leads to an only partial restoration of H60 expression on the cell surface, suggesting the involvement of another, so far unknown, viral inhibitor. In spite of this, an m155 deletion mutant virus shows NK cell-dependent attenuation in vivo. The acquisition of endo-ß-N-acetylglucosaminidase H resistance and the preserved half-life of H60 in MCMV-infected cells indicate that the m155-mediated effect must take place in a compartment after H60 exits from the ERGIC-cis-Golgi compartment.

* Corresponding author. Mailing address: Department of Histology and Embryology, Faculty of Medicine, University of Rijeka, B. Branchetta 20, 51000 Rijeka, Croatia. Phone: 385 51 651 206. Fax: 385 51 651 176. E-mail: jstipan{at}medri.hr.

{dagger} Present address: Institute for Virology, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany.

Journal of Virology, March 2005, p. 2920-2930, Vol. 79, No. 5
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.5.2920-2930.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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