CCL8 and disease arising from reactivation of latent virus: We now show that, during latent infection of myeloid cells, LAcmvIL-10 mediates the known latency-associated increase in secreted cellular CCL8 and that this is due to concomitant suppression by LAcmvIL-10 of expression of the cellular miRNA hsa-miR-92a, which in itself contributes to a number of effects during latency (15), as well as targeting CCL8 directly.