However, an increase in secreted CCL2 was also observed from latently infected GMPs, and related to the stimulation of CD14+ monocytes migration toward the site of latency (Stern and Slobedman, 2008); whereas secretion of both CCL2 and CCL8 was measured during a short-term experimental latent infection of CD14+ monocytes, and linked to the recruitment of CD14+ monocytes and CD4+ Th1 cells to latently infected cells (Noriega et al., 2014). Here, CCL2 is linked to disease arising from reactivation of latent virus.