The response to TLR ligation of human CD16+CD14− monocytes is weakly modulated as a consequence of persistent infection with the hepatitis C virus

Little is known about the frequency and function of CD16+CD14− monocytes from chronic HCV patients. We observed that the absolute numbers and ratio of CD16+CD14− to CD14+CD16− monocytes were similar between chronic HCV patients and healthy individuals. Functionally, we found that CD16+CD14− monocytes are more responsive to TLR8-ligation and only weakly responsive to LPS stimulation in producing TNF as compared to CD14+CD16− monocytes. We found no overt impairment of the function of CD16+CD14− monocytes from patients, except for an augmented induction of MIP-1β-producing CD16+CD14− monocytes upon TLR4-ligation. However, the increased frequency of MIP-1β-producing CD16+CD14− monocytes was not associated with viral load, ALT or fibrosis level. Our findings indicate that, different from other infectious diseases, the frequency and function of CD16+CD14− monocytes are only minimally altered as a consequence of the persistent state of HCV infections, and our findings therefore do not suggest a role for CD16+CD14− monocytes in HCV pathogenesis.

► The function of CD16+CD14+ monocytes from chronic HCV patients and controls is examined.
► CD16+CD14+ monocytes strongly respond to TLR8 agonists, but weakly to TLR4 agonists.
► The frequency of CD16+CD14+ monocytes is not changed in chronic HCV patients.
► Also, no overt modulation of their function in patients is observed.
► A role of CD16+CD14+ monocytes in HCV pathogenesis is therefore not suggested.