<i>GSTT1</i>and<i>GSTM1</i>Null Genotypes May Facilitate Hepatitis C Virus Infection Becoming Chronic

Martı́nez, Carmen; García‐Martín, Elena; Ladero, José M.; Herráez, Óscar; Ortega, Luís; Taxonera, Carlos; Suárez, África Peral; Dı́az-Rubio, Manuel; Agúndez, José A. G.

doi:10.1086/513569

Cited by 18 publications

(15 citation statements)

References 15 publications

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“…In addition, we investigated whether GSTT1 and GSTM1 gene variations play a role in liver fibrosis caused by hepatitis C virus and found that individuals with the null variant of both GSTT1 and GSTM1 have considerably increased risk of advanced fibrosis. This result was in agreement with a previous study in Spain (27). Martinez et al recruited 139 HCV-infected Spanish patients and 329 healthy controls to estimate the association between both gene polymorphisms and chronic phase of HCV-induced liver disease.…”

Section: Discussionsupporting

confidence: 92%

“…Thus, genetic polymorphisms of antioxidant enzymes could modify the capacity to alleviate oxidative stress and thereby influence the progression of liver damage. However, there have been few studies on the effects of GST gene polymorphism on the disease progression of HBV infection (25,26), but so far we have not seen any reports about that association in the investigation of the relationship between GST gene polymorphism and stage of liver fibrosis in HCV-infected patients in Taiwan, only one report in Spain (27).…”

Section: Introductionmentioning

confidence: 99%

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Glutathione-S-Transferase M1 and T1 Gene Polymorphisms and Susceptibility to the Progression of Liver Fibrosis in Hcv-Infected Patients in Taiwan

Sun¹,

Jeng²,

Lee³

et al. 2014

Journal of Medical Biochemistry

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SummaryBackground: This study was conducted to evaluate the influence of glutathione-S-transferase (GST) M1 and T1 polymorphisms in 184 patients with different stages of liver fibrosis and hepatitis C virus infection and 173 healthy control subjects. Methods: DNA samples were extracted from whole blood, and the polymorphisms of GSTM1 and GSTT1 were determined with PCR using fluorescence-labeled Taq Man probes. Associations between specific genotypes and progression of liver fibrosis were examined by use of the logistic regression analysis to calculate the odds ratio (OR) and 95% confidence intervals (CI). Results: Results show that no differences were found between the frequencies of GSTM1 (49.8% versus 50.2%) and GSTT1 (52.2% versus 47.8%) null genotypes in HCV-infected pa tients and healthy controls, respectively. In addition, there was also no significant relation between the frequency of GSTM1 or GSTT1 gene polymorphisms and fibrosis stage as classified by the METAVIR group. Conclusions: The combined GSTM1 and GSTT1 null genotypes showed an association between GSTM1 [-]/GSTT1 [-] and progression of liver fibrosis.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Glutathione-S-Transferase M1 and T1 Gene Polymorphisms and Susceptibility to the Progression of Liver Fibrosis in Hcv-Infected Patients in Taiwan

Sun¹,

Jeng²,

Lee³

et al. 2014

Journal of Medical Biochemistry

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“…Our study showed a marked excess of the combined GSTM1/GSTT1 double‐null genotype in the case of chronic HCV Egyptian patients compared with a healthy control group. This is in accordance with the results obtained in Spanish (Martinez et al., ) and Taiwanese studies (Sun et al., ).…”

Section: Discussionsupporting

confidence: 93%

Glutathione S-Transferase M1 and T1 Gene Polymorphisms and the Outcome of Chronic Hepatitis C Virus Infection in Egyptian Patients

Ibrahim

Ahmed

Alazizi

et al. 2015

Annals of Human Genetics

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We analysed the distribution of GSTM1 and GSTT1 gene polymorphisms in Egyptian patients with chronic hepatitis C, and investigated their relationship to the clinical outcome of chronic hepatitis C virus (HCV) infection. This study included 169 patients with chronic HCV infection and 145 healthy and matched controls.GSTM1 and GSTT1 polymorphisms were genotyped by multiplex polymerase chain reaction. Individual GSTM1 null and GSTT1 null genotypes were more frequent in patients versus control subjects [OR, 4 (95% CI, 2.5-6.4); P ˂ 0.001] and [OR, 1.7 (95% CI, 1.1-2.6); P = 0.025], respectively. The patient group showed a higher frequency of the combined GSTM1/GSTT1 double-null genotype than the control group [OR, 1.8 (95% CI, 1.1-2.9); P = 0.016]. The distribution frequencies of the combined GSTM1/GSTT1 double-null genotype were significantly different [OR, 0.5 (95% CI, 0.25-0.99); P = 0.049] between F0-F3 and F4. There were no significant differences between the two groups with regard to other genotypes. The combined GSTM1/GSTT1 double-null genotype was significantly increased in Child-Pugh C patients in comparison to Child-Pugh A+B (P = 0.02). There was no significant difference between different classes with regard to other genotypes. In conclusion, we identified an association between the combined GSTM1/GSTT1 double-null genotype and advanced liver fibrosis and outcome of chronic HCV infection in Egyptian patients.

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“…Another effect that ROS appear to have on HCV is an increase in HCV genome heterogeneity, which may contribute to the evolutional survival of the virus by ensuring viral escape from the immune system (during establishment of infection as well as during treatment) [158, 159]. Indeed, patients with a null genotype of glutathione-S-transferases, namely gstt1 and gstm1 , are characterized by decreased rates of the spontaneous resolution of acute HCV infection [160]. …”

Section: Hepatitis C Virusmentioning

confidence: 99%

Oxidative stress, a trigger of hepatitis C and B virus-induced liver carcinogenesis

et al. 2016

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Virally induced liver cancer usually evolves over long periods of time in the context of a strongly oxidative microenvironment, characterized by chronic liver inflammation and regeneration processes. They ultimately lead to oncogenic mutations in many cellular signaling cascades that drive cell growth and proliferation. Oxidative stress, induced by hepatitis viruses, therefore is one of the factors that drives the neoplastic transformation process in the liver. This review summarizes current knowledge on oxidative stress and oxidative stress responses induced by human hepatitis B and C viruses. It focuses on the molecular mechanisms by which these viruses activate cellular enzymes/systems that generate or scavenge reactive oxygen species (ROS) and control cellular redox homeostasis. The impact of an altered cellular redox homeostasis on the initiation and establishment of chronic viral infection, as well as on the course and outcome of liver fibrosis and hepatocarcinogenesis will be discussed The review neither discusses reactive nitrogen species, although their metabolism is interferes with that of ROS, nor antioxidants as potential therapeutic remedies against viral infections, both subjects meriting an independent review.

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GSTT1andGSTM1Null Genotypes May Facilitate Hepatitis C Virus Infection Becoming Chronic

Cited by 18 publications

References 15 publications

Glutathione-S-Transferase M1 and T1 Gene Polymorphisms and Susceptibility to the Progression of Liver Fibrosis in Hcv-Infected Patients in Taiwan

Glutathione-S-Transferase M1 and T1 Gene Polymorphisms and Susceptibility to the Progression of Liver Fibrosis in Hcv-Infected Patients in Taiwan

Glutathione S-Transferase M1 and T1 Gene Polymorphisms and the Outcome of Chronic Hepatitis C Virus Infection in Egyptian Patients

Oxidative stress, a trigger of hepatitis C and B virus-induced liver carcinogenesis

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