Assessment of Anti-Toxoplasma gondii Antibodies in Patients with Chronic Hepatitis C Virus Infection: Evaluation of Liver Fibrosis Biomarkers and Elastography Findings

Background: Chronic hepatitis C virus (HCV) infection remains an important cause of progressive liver disease and fibrosis. Toxoplasma gondii infection is highly prevalent worldwide and may influence inflammatory and fibrotic pathways; however, its clinical significance in patients with chronic HCV infection remains unclear. This study aimed to assess the prevalence of anti-T. gondii antibodies among patients with chronic HCV infection and to evaluate potential differences in liver fibrosis biomarkers and elastography findings according to T. gondii serostatus. Methods: In this case–control study conducted between December 2023 and October 2024 at Beni-Suef University Hospital, Beni-Suef, Egypt, 58 treatment-naive patients with chronic HCV infection, confirmed by documented anti-HCV positivity together with detectable serum HCV RNA, and 20 healthy controls were enrolled. Anti-T. gondii IgG and IgM antibodies were detected using a qualitative rapid immunochromatographic assay (OnSite Toxo IgG/IgM Combo Rapid Test, CTK Biotech, Poway, CA, USA). In HCV patients, liver fibrosis was assessed using transient elastography and circulating fibrosis-related biomarkers, including tissue inhibitor of metalloproteinase-1 (TIMP-1), macrophage colony-stimulating factor (M-CSF), and YKL-40, the latter three measured by quantitative sandwich enzyme-linked immunosorbent assay. Clinical, biochemical, and fibrosis-related parameters were compared between HCV patients and controls and according to T. gondii serological status. Results: Anti-T. gondii IgG seropositivity was detected in 26/58 (44.8%) patients with chronic HCV infection and 8/20 (40.0%) healthy controls, whereas IgM seropositivity was observed in 4/58 (6.9%) and 2/20 (10.0%), respectively. No statistically significant differences were observed between patients and controls in either IgG or IgM seropositivity rates. Patients with chronic HCV infection showed significantly higher circulating concentrations of TIMP-1, M-CSF, and YKL-40 than healthy controls (all p < 0.001). Among HCV patients, anti-T. gondii IgG serostatus was not significantly associated with FibroScan-defined fibrosis category, platelet count, AST, GGT, TIMP-1, M-CSF, or YKL-40. Analyses involving IgM-positive patients were considered exploratory because of the small number of IgM-positive participants. Conclusions: Anti-T. gondii IgG and IgM seropositivity did not differ significantly between patients with chronic HCV infection and healthy controls. Among HCV patients, serological evidence of previous T. gondii exposure was not significantly associated with transient elastography-defined fibrosis severity or the evaluated circulating fibrosis biomarkers. Because seropositivity reflects exposure rather than active parasitic infection, the findings should not be interpreted as evidence of active hepatic toxoplasmosis. Larger multicenter longitudinal studies incorporating molecular confirmation of active T. gondii infection are warranted.