Author:
Santiago Angélica Menezes,da Silva Graça Amoras Ednelza,Queiroz Maria Alice Freitas,da Silva Conde Simone Regina Souza,Cayres-Vallinoto Izaura Maria Vieira,Ishak Ricardo,Vallinoto Antonio Carlos Rosário
Abstract
Abstract
Background
Genetic changes may induce dysregulated cytokine production and affect the progression of the chronic disease caused by the hepacivirus C (HCV) because the balance of pro- and anti-inflammatory cytokines determines the outcome of infection. This study evaluated the TNFA -308G>A and IL10 -1082A>G polymorphisms in the susceptibility and progress of chronic hepatitis C.
Method
The study included 101 samples from patients with chronic hepatitis C and 300 samples from healthy donors. Polymorphisms were typed by real-time PCR and were analyzed for associations with histopathological parameters (according to METAVIR classification) and HCV viral load.
Results
The polymorphic genotype for the TNFA -308G>A variant was not present in the group of patients with chronic hepatitis C and its absence could be associated with protection against HCV infection (p = 0.0477). Patients with the polymorphic genotype of the IL10 -1082A>G polymorphism had higher HCV viral load than wild-type patients (p = 0.0428). Neither polymorphism was associated with different levels of necroinflammatory activity or fibrosis scores.
Conclusion
Our results suggest the polymorphic genotype at TNFA -308G>A as protective against chronic HCV infection, and the polymorphic genotype at the IL10 -1082A>G variant associated with higher HCV viral load. Further studies must be performed in order to confirm these associations.
Funder
Conselho Nacional de Desenvolvimento Científico e Tecnológico
Publisher
Springer Science and Business Media LLC
Cited by
6 articles.
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