Hepatitis G virus infection in chronic hepatitis C: frequency, features and response to interferon therapy

• Published in: Journal of hepatology 1997-04, Vol.26 (4), p.787-793
• Main Authors: Sáiz, Juan Carlos, Ampurdanés, Sergi, Olmedo, Eva, López-Labrador, Francesc Xavier, Forns, Xavier, Guilera, Magdalena, Tassies, Dolors, Costa, Josep, Sánchez-Tapias, José María, Jiménez de Anta, María Teresa, Rodés, Juan
• Format: Article
• Language: English
• Subjects: Adult; Antiviral Agents - therapeutic use; Biological and medical sciences; Chronic Disease; Chronic hepatitis; Female; Flaviviridae - genetics; Flavivirus; Hepacivirus - genetics; Hepatitis C - complications; Hepatitis, Viral, Human - complications; Hepatitis, Viral, Human - epidemiology; Hepatitis, Viral, Human - therapy; Human viral diseases; Humans; Infectious diseases; Interferons - therapeutic use; Male; Medical sciences; Middle Aged; Prevalence; RNA, Viral - analysis; Treatment Outcome; Viral diseases; Viral hepatitis
• ISSN: 0168-8278; 1600-0641
• DOI: 10.1016/S0168-8278(97)80243-7

Background/Aims: The pathogenic relevance of the hepatitis G virus (HGV) and its sensitivity to interferon are currently under investigation. This study aimed to investigate the prevalence of HGV infection in patients with chronic hepatitis C and to elucidate if HGV co-infection modifies the clinical course and the response to interferon therapy in this disease. Methods: HGV-RNA was investigated by reverse transcription-polymerase chain reaction in serum from 143 consecutive patients who received interferon α-2b (3 MU t.i.w.) for 24 weeks. Baseline features and response to therapy in HGV-infected and non-infected patients were compared. To assess the antiviral effect of interferon, serial quantitative measurement of HCV-RNA and HGV-RNA in serum was performed in patients co-infected with HCV and HGV. Results: Eight patients (5.6%) presented HGV-RNA sequences in serum. No significant differences were found between HGV-infected and non-infected patients in relation to age, sex, source of infection, liver function tests, liver histology and HCV genotype, nor in the biochemical response to interferon, which was sustained in 12% and 15%, transient in 37% and 30% and absent in 50% and 55% of HGV-infected and non-infected patients, respectively. HGV-RNA became negative in all treated patients, but sustained viral inhibition was observed only in those with low viral load. Conclusions: The prevalence of HGV infection in HCV-infected patients is relatively low in our geographical area. HGV co-infection does not appear to modify the clinical presentation nor the response to interferon in chronic hepatitis C. HGV is sensitive to interferon, particularly if pre-treatment viral load is low.