Viral hepatitis B (HBV) and C (HCV) are major global public health problems, with high prevalence in Northern Brazil. Because they share common transmission routes, HBV/HCV coinfection is uncommon and results in complex virological interactions that can influence viral replication kinetics and modulate the host immune response. Understanding the imbalance between pro-inflammatory and anti-inflammatory cytokines, as well as viral replication in these infections, is essential for therapeutic and prognostic optimization. The objective of this study is to characterize plasma viral load and the profile of inflammatory cytokines (IL-6, TNF-α, IL-10, and IFN-γ) in groups of patients with HBV and HCV mono-infection and coinfection treated at a reference unit.

Cross-sectional study conducted using biological samples from patients treated at a Reference Unit between December 2017 and August 2019. Detection and quantification of HBV DNA (HBV-DNA) were performed by real-time PCR, and HCV RNA (HCV-RNA) by real-time RT-PCR. Plasma concentrations of IL-6, TNF-α, IL-10, and IFN-γ were determined using the Luminex platform (Bio-Plex system).

Higher viral loads were observed in the mono-infected groups: median HCV-RNA 6.1 log10 IU/mL vs. 5.5 log10 IU/mL in coinfection (p = 0.0001); HBV-DNA 2.1 log10 IU/mL vs. 1.4 log10 IU/mL in coinfection (p=0.0005). HCV mono-infected patients had significantly elevated levels of TNF-α, IFN-γ, and IL-10 (p=0.005; p=0.0004; p=0.002, respectively) compared with the other groups.

The results demonstrate replicative dominance of HCV in both mono-infection and coinfection scenarios, although in coinfection there is suppression of both viruses, suggesting modulation of one virus over the other. The inflammatory profile observed in HCV mono-infection, characterized by concomitant elevation of both pro- and anti-inflammatory cytokines, suggests a persistent immune response and a possible correlation with greater aggressiveness of liver disease. These findings contribute to the understanding of immunopathological mechanisms in viral coinfection and may support personalized therapeutic strategies in regions of high endemicity.