To test if β2.7 has a protective role during latent infection, we stressed infected monocytes with cadmium chloride (CdCl2), which is an established way of causing apoptosis in primary lymphocytes and monocytes by inducing loss of mitochondrial membrane potential (MMP) [22,23]; similar effects have also been demonstrated in monocytic U937 and THP-1 cell lines [24,25]. This evidence concerns the gene MRAP and disease arising from reactivation of latent virus.