In conclusion, we believe that changes in myeloid-specific HCLS1 imparted by latent infection of monocytes with HCMV can alter their adhesion to endothelial cells and promote transendothelial migration and that this could aid efficient dissemination of HCMV latently infected cells from the peripheral blood to potential tissue sites of reactivation. The gene discussed is HCLS1; the disease is disease arising from reactivation of latent virus.