In addition, studies using the clinical isolate stain of HCMV Merlin, showed that the lack of UL111A led to a decrease in the establishment of latent infection of CD14+ monocytes, as well as in latently infected CD34+cells (Poole et al., 2014), suggesting that LAcmvIL10 may play a role in the establishment and/or maintenance of latency. This evidence concerns the gene CD14 and disease arising from reactivation of latent virus.