The Gammaherpesvirus M3 Protein

100-fold less virulent [39] and the M3 protein was suggested to act by altering the nature of the associated inflammation infiltrate from a lymphocyte- and monocyte-rich infiltrate to one composed mainly of neutophils. 

As described before, chemokine inhibition may be a useful approach for the prevention of restenosis after coronary surgery or atherosclerosis. This concept has been further substantiated in vivo through the use of the broad spectrum vCKBP M3. Thus, systemic M3 expression from a transgene, or delivery of recombinant M3 protein, have been shown to reduce intimal hyperplasia after femoral artery injury [40] and aortic allograft transplantation [25], respectively. 

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Figure 16.1 Mechanisms of chemokine inhibition by the CKBPs encoded by pathogens. Chemokines interact with CACs present at the surface ofendothelial cells and are presented to the leukocytes. The chemokine receptors expressed at the surface of leukocytes interact with chemokines and intracellular signaling is triggered to induce cell migration. The CKBPs may have broad chemokine binding specificity, such as the poxvirus 35-kDa protein, the gammaherpesvirus M3 protein orthe MYXVM-...

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