Hepatitis C virus (HCV) infection is an important public health problem. According to estimates, the prevalence of hepatitis C worldwide is approximately 1 %, affecting more than 58 million individuals and being responsible for 242,000 deaths in 2022, mainly from cirrhosis and hepatocellular carcinoma [1]. HCV is classified in the Flaviviridae family, Hepacivirus genus, with 8 genotypes and 90 subgenotypes well characterized to date. Acute infection is generally asymptomatic [2].

However, the inability of the immune system to eliminate the pathogen usually results in the development of a persistent viral infection, favorable for chronic progression in 80 % of infected cases [3]. Viral persistence is attributed to its ability to escape immunological surveillance through modulation of immune cell activity, responsible to produce inflammatory mediators that establish a favorable microenvironment for immune evasion and viral persistence [4]. Recruitment and intralobular infiltration of peripheral blood cells can play an important role in immunopathogenesis, considering that increasing the number of cells is associated with liver tissue damage [5].

Monocytes play an important role in homeostasis, host defense, inflammation resolution, and tissue repair. Subpopulations of circulating monocytes are defined by the expression of CD14 and CD16 present in cells. CD14HighCD16− (classic) monocytes represent the largest percentage of monocytes in the peripheral circulation responsible for migrating to tissues and controlling persistent inflammatory processes or differentiating into intermediate CD14++CD16+ monocytes in the peripheral circulation [6]. CD14LowCD16++ (nonclassical) monocytes are the smallest population, recognized for patrolling blood vessels and promoting tissue regeneration and homeostasis [7].

The direct acting antivirals (DAA) therapy for HCV infection became available in 2014 and provided a major advance in the eradication of HCV and control of the disease [8]. However, disease progression remains a problem for patients with chronic hepatitis C, which makes it important to study the cellular populations and immunological mediators involved in the pathogenesis of chronic liver disease. Our objective was to evaluate the frequency of peripheral monocyte subpopulations and the expression of circulating inflammatory mediators in chronic hepatitis C patients with different degrees of liver fibrosis treated with DAA.