Bhargavan and colleagues suggested that the co-infection with RNA viruses such as HCV might contribute to HIV replication and pathogenesis via epigenetic alterations in myeloid cells of HIV + individuals: In vitro stimulation of latent HIV + monocytic cell lines with ligands of the Toll-like receptor 3 (TLR3), a sensor of foreign nucleic acid structures, was shown to rapidly induce acetylation of the integrated HIV promoter [80]. The gene discussed is TLR3; the disease is coinfection.