The aim: to analyse the dynamics of TGF-1β and MMP-9 in the blood serum of patients with chronic hepatitis C (HCV) infected with HCV GT1 on the background of antiviral treatment depending on the severity of liver fibrosis.

Materials and methods. The study included 92 patients with GT1 HCV infection treated with antiviral therapy (AVT) – OBV / PTV / r+DSV±RBV. The severity of liver fibrosis was determined by elastometry. The content of TGF-1β (Elabscience, USA) and MMP-9 (Elabscience, USA) in the blood serum was determined by ELISA.

Results. In patients with CHC GT1 before the start of AVT, profibrogenic potential prevailed: increased TGF-1β (p < 0.05), decreased MMP-9 (p < 0.05) and a higher TGF-1β / MMP-9 ratio (p < 0.05). AVT (OBV / PTV / r+DSV±RBV) slows down fibrogenesis and activates antifibrotic processes, which is confirmed by an increase in MMP-9 (p < 0.05) and a decrease in TGF-1β / MMP-9 (p < 0.05) compared to the pre-treatment values. Prior to AVT, patients with GT1 HCV with liver fibrosis F 0–2 had lower MMP-9 levels (p < 0.05) than healthy subjects, with no changes in TGF-1β and TGF-1β / MMP-9 ratio (p > 0.05). In patients with F 3–4 liver fibrosis, serum TGF-1β and the TGF-1β / MMP-9 ratio were higher, and MMP-9 was lower, both compared with healthy subjects (p < 0.05) and compared with patients with F 0–2 (p < 0.05). In patients with F 0–2, at the time of completion of AVT, the studied parameters do not differ from healthy individuals (p > 0.05). In patients with F 3–4 at the time of completion of AVT, the TGF-1β / MMP-9 ratio remains higher both in comparison with healthy individuals (p < 0.05) and in comparison with patients with CHC GT1 with liver fibrosis F 0–2 (p < 0.05).

Conclusions. We demonstrated more significant dynamics of antifibrotic changes during direct-acting antiviral agents based AVT in patients with GT1 CHC in the presence of F 0–2 liver fibrosis compared to patients with F 3–4.