Chronic hepatitis C virus infection impairs natural killer cells–dendritic cells cross‐talk: An in vitro culture study

To examine the cross-talk between NK cells and DCs in hepatitis C virus (HCV) infection, we isolated monocytes from 20 chronic HCV patients healthy controls. Monocytes were used to generate immature which pulsed with peptides (core, NS3–NS4, NS5). Four different cocultures carried out: E1, both a patient; E2, control cocultured E3, patient control; E4, control. Using flow cytometry, assessed effect of these on levels maturation markers activation/inhibition cells. Results showed that peptide-pulsed defect form decreased HLA-DR, CD86, increased CD83 expression especially when NK. This was mainly due core peptide pulsing lesser extent NS5 pulsing, whereas there no NS3–NS4 pulsing. Alternatively, upregulated activation inhibition DCs. Compared E1 resulted higher apoptosis percentage than Taken together, data indicate infection impairs NK–DC may be leading cause viral persistence chronicity.