“…However, rather than enhancing chemokine binding, the Y80A mutation paradoxically resulted in loss of the ability of vCCI to inhibit CCL5 activity, presumably because the Y80A vCCI variant was no longer able to bind the chemokine [ 34 ]. The question of why the Y80A vCCI variant unexpectedly has weaker chemokine binding is currently being addressed computationally and in ongoing experiments [ [66] , [67] , [68] ].…”