IL23A and chronic hepatitis B virus infection: Our results also suggested that the activity of the proinflammatory IL-23/IL-17 signaling pathway is not been efficiently controlled by the host inhibitory machinery, in this case the Treg (Foxp3) cells; the constitutive activation of the IL-23/IL-17 signaling pathway may partially explain the HBV persistence that occurs in the chronic hepatitis B state.