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

<table>MCMV-encoded proteins disrupt NK-cell recognition of infected cells. During MCMV infection, the surface expression of the  stress-induced molecules, ligands for NKG2D, is downregulated: m152 downregulates all isoforms of RAE-1, m145 and m155 interfere with  H60 and MULT-1, respectively, and m138 downregulates H60, MULT-1, and RAE-1<i>ε</i> (a). m157 binds both inhibitory NK receptor, Ly49I, and activating NK receptor, Ly49H (b).</table>

BioMed Research International

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Figure 1: How the Virus Outsmarts the Host: Function and Structure of Cytomegalovirus MHC-I-Like Molecules in the Evasion of Natural Killer Cell Surveillance 

Figure 1 | How the Virus Outsmarts the Host: Function and Structure of Cytomegalovirus MHC-I-Like Molecules in the Evasion of Natural Killer Cell Surveillance 