Serum Galectin-3 in Hepatitis C Virus Infection Declines after Successful Virus Eradication by Direct-Acting Antiviral Therapy

Abstract

Background and Aims: Serum galectin-3 is regarded as an inflammatory marker in patients with chronic liver diseases. Hepatitis C virus (HCV) infection is associated with higher levels of inflammatory molecules which ameliorate by efficient treatment with direct-acting antivirals (DAAs). The aim of this study was to compare serum galectin-3 levels between HCV patients before treatment with DAAs and at the time of sustained virologic response at 12 weeks post-treatment (SVR12).
 Methods: Hepatitis B and human immunodeficiency virus-negative HCV infected patients not treated with HCV therapies before were recruited at the University Hospital of Regensburg. Galectin-3 was measured by enzyme-linked immunosorbent assay in the serum of patients with chronic HCV infection, before treatment initializing, at four and twelve weeks after the start of DAA therapy and at SVR12. Associations of serum galectin-3 with C-reactive protein (CRP), leukocyte count and measures of liver disease severity were analyzed. Liver fibrosis was assessed by acoustic radiation force impulse, the aspartate aminotransferase/platelet ratio index, and the fibrosis-4 score.
 Results: In the serum of 81 HCV patients, galectin-3 did not correlate with viral load, viral genotype, CRP, leukocyte count, or the model for end stage liver disease score. Therapy with DAAs effectively diminished viral load within four weeks in all patients. The median value of the serum galectin-3 was 3.0 (Q1:2.0, Q3:4.0) ng/ml before therapy and declined to 2.4 (Q1: 1.7, Q3: 3.4) ng/ml at SVR12 (p<0.001; paired samples of 67 patients). At SVR12, serum galectin-3 was not correlated with CRP (r=0.057, p=0.646) or leu-kocyte count (r=0.222, p=0.071) and did not change with increasing fibrosis stage. The associations between serum galectin-3 and body mass index, liver steatosis or diabetes could not be observed.
 Conclusions: Elimination of HCV by DAA treatment lowered serum galectin-3 compared to the pre-treatment levels suggesting that HCV infection causes an increase of this immune-regulatory protein.

Adipokines as Diagnostic and Prognostic Markers for the Severity of COVID-19

“…Galectin-3 was also shown to upregulate antiviral genes to inhibit influenza A virus replication [138]. Moreover, galectin-3 expression is induced in immune cells infected by HIV or human T lymphotropic virus type I [138] and upregulated in the serum of HCV-infected patients [138,143]. While the consequences of infection-related elevation of galectin-3 levels remain to be fully understood, galectin-3 upregulation enhanced inflammatory cytokine levels and myofibroblast activation, both with roles in lung fibrosis [144].…”

Increased Levels of Galectin-3 in Critical COVID-19

“…Concerning the role of galectin-3 in viral infections, it can participate in interactions taking place between virus and host during viral entry, viral replication, or immune response modulation [7]. Hepatitis C virus infection increases serum galectin-3 levels, which in turn can promote inflammation and fibrosis progression [22]. Galectin-3 is also suggested to play a role in the early stages of human immunodeficiency virus (HIV) infection by enhancing viral entry [23].…”

The Pivotal Role of Galectin-3 in Viral Infection: A Multifaceted Player in Host–Pathogen Interactions

“…Galectin-3 has also been implicated in HCV infection. Research comparing serum levels of Gal-3 in HCV patients before and after treatment with direct-acting antivirals (DAAs) has shown that HCV infection increases serum Gal-3 levels, which may contribute to inflammation and fibrosis progression [96]. However, successful DAA treatment reduces serum Gal-3 levels, suggesting a potential role for Gal-3 in monitoring HCV treatment outcomes [96].…”