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Oxidative stress response in patients infected by diverse hepatitis C virus genotypes
Mohammad Hassan Khadem Ansari1, Mir-Davood Omrani2, Fatemeh Kheradmand3
1Clinical Biochemistry Department, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, IR Iran.
Insights
Hepatitis C virus (HCV) genotypes significantly impact oxidative stress levels. Genotype 1a/1b is linked to severe oxidative stress, while other genotypes show milder responses, suggesting tailored therapies.
Area of Science:
- Hepatology
- Virology
- Biochemistry
Background:
- The precise molecular mechanisms driving hepatitis C virus (HCV) pathogenesis are not fully understood.
- Oxidative stress is a known factor in chronic HCV infection, but its correlation with specific HCV genotypes requires further investigation.
Purpose of the Study:
- To investigate the impact of different HCV genotypes on oxidative status.
- To compare oxidative stress markers between HCV patients and healthy controls.
Main Methods:
- A case-control study involving 160 HCV patients with known genotypes and 160 healthy controls.
- Measurement of oxidative stress markers: total antioxidant status (TAS), glutathione (GSH and GSSG), Gamma-glutamyl transferase (GGT), and malondialdehyde (MDA).
Main Results:
- Significant differences in all measured oxidative stress markers were observed between HCV patients and controls (P < 0.05).
- Distinct patterns of oxidant/antioxidant balance were identified across various HCV genotypes.
- An increasing trend in antioxidant levels and a decreasing trend in oxidative markers (except MDA) were noted from genotype 1a/1b towards healthy controls.
Conclusions:
- HCV genotype 1a/1b may be associated with more severe oxidative stress and potentially more serious disease.
- Milder oxidative responses were observed in genotypes 4, 2a/c, 2b, and 3a.
- Combined antiviral and antioxidative therapies could improve treatment outcomes for HCV patients, particularly those with more aggressive genotypes.
Background:
The molecular mechanism of hepatitis C-virus (HCV) genome-specific pathogenesis remains unclear. Oxidative stress is an important pathophysiological mechanism in chronic HCV infection, but its relation to HCV genotypes has not been thoroughly examined.
Objectives:
In the present case-control study, the effect of diverse HCV genotypes on oxidative status changes was investigated.
Patients And Methods:
From 310 patients examined by enzyme immunoassay and PCR, 160 patients with positive results for HCV with previously determined genotypes were chosen. For the control group, 160 first time blood donors referred to the Regional Blood Transfusion organization of the West Azerbaijan province, northwestern Iran were selected. Oxidative stress markers such as total antioxidant status (TAS), serum levels of reduced (GSH) and oxidized (GSSG) glutathione, Gamma-glutamyl transferase (GGT) and malondialdehyde (MDA) were evaluated in patients infected with diverse HCV genotypes and those in the control group.
Results:
In the patient and control groups, the mean ± SE of TAS, GSH, GSSG, GGT and MDA were 1.04 ± 0.35 vs. 2.68 ± 0.77, 1.25 ± 0.37 vs. 3.12 ± 0.58, 0.20 ± 0.05 vs. 0.08 ± 0.04, 26.82 ± 5.62 vs 8.28 ± 2.03 and 2.56 ± 0.60 vs. 0.93 ± 0.34. All markers had statistical difference between the two groups (P <0.05). Obvious differences were found in oxidant/antioxidant balance among diverse HCV genotypes with an ascending trend in antioxidant levels among patients infected with genotypes 1a/b, 4, 2a/c, 2b, 3a and healthy controls and a vice versa trend in measures of oxidative markers except for malondialdehyde with a variable pattern.
Conclusions:
More serious disease in HCV genetic subtype 1a/1b might be associated with more severe oxidative stress. Milder damage in subtypes 4, 2a/c, 2b and 3a could be related to lower oxidative response, respectively. A combination of antiviral and antioxidative therapies may enhance the overall response rate of patients with HCV infection, especially with more destructive genotypes.
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