The IL6-174G/C Polymorphism Associated with High Levels of IL-6 Contributes to HCV Infection, but Is Not Related to HBV Infection, in the Amazon Region of Brazil
Maria Alice Freitas Queiroz,
Angélica Menezes Santiago,
Tuane Carolina Ferreira Moura,
Ednelza da Silva Graça Amoras,
Simone Regina Souza da Silva Conde,
Izaura Maria Vieira Cayres-Vallinoto,
Ricardo Ishak,
Antonio Carlos Rosário Vallinoto
Affiliations
Maria Alice Freitas Queiroz
Laboratory of Virology, Institute of Biological Sciences, Federal University of Pará (UFPA), Belém 66075-110, Brazil
Angélica Menezes Santiago
Laboratory of Virology, Institute of Biological Sciences, Federal University of Pará (UFPA), Belém 66075-110, Brazil
Tuane Carolina Ferreira Moura
Laboratory of Virology, Institute of Biological Sciences, Federal University of Pará (UFPA), Belém 66075-110, Brazil
Ednelza da Silva Graça Amoras
Laboratory of Virology, Institute of Biological Sciences, Federal University of Pará (UFPA), Belém 66075-110, Brazil
Simone Regina Souza da Silva Conde
Pathology Service, João de Barros Barreto University Hospital, Federal University of Pará (UFPA), Belém 66073-000, Brazil
Izaura Maria Vieira Cayres-Vallinoto
Laboratory of Virology, Institute of Biological Sciences, Federal University of Pará (UFPA), Belém 66075-110, Brazil
Ricardo Ishak
Laboratory of Virology, Institute of Biological Sciences, Federal University of Pará (UFPA), Belém 66075-110, Brazil
Antonio Carlos Rosário Vallinoto
Laboratory of Virology, Institute of Biological Sciences, Federal University of Pará (UFPA), Belém 66075-110, Brazil
The dysregulation of cytokine production can lead to an inefficient immune response, promoting viral persistence that induces the progression of chronic viral hepatitis. The study investigated the association of the IL6-174G/C polymorphism with changes in cytokine levels and its influence on the persistence and progression of chronic hepatitis caused by HBV and HCV in 72 patients with chronic hepatitis B (HBV), 100 patients with hepatitis C (HCV), and a control group of 300 individuals. The genotyping of the IL6-174G/C polymorphism was performed by real-time PCR, and cytokine levels were measured by enzyme-linked immunosorbent assay (ELISA). HCV patients with the wild-type genotype (GG) had a higher viral load (p = 0.0230). The plasma levels of IL-6 were higher among patients infected with HBV and HCV than among the control group (p p p = 0.0286), which were associated with A2–A3 inflammatory activity (p = 0.0097). Patients with A2–A3 inflammatory activity and GG genotype had higher levels of IL-6 than those with the GC/CC genotype (p = 0.0127). In conclusion, the wild-type genotype for the IL6-174G/C polymorphism was associated with high levels of IL-6 and HCV viral load and inflammatory activity, suggesting that this genotype may be a contributing factor to virus-induced chronic infection.