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Possible association between serum GB virus C RNA level and disease activity in fulminant hepatitis type G
K Inoue1, M Yoshiba, K Sekiyama
1Division of Gastroenterology, Showa University Fujigaoka Hospital, Yokohama, Japan.
Insights
GB virus C RNA levels correlated with liver damage in patients with fulminant hepatitis. This suggests GB virus C may cause severe liver disease, not just be a bystander.
Area of Science:
- Hepatology
- Virology
- Molecular Biology
Background:
- The etiological role of GB virus C (GBV-C) in severe liver disease, particularly fulminant hepatitis, remains debated.
- This study investigated a potential causal link between GBV-C infection and fulminant hepatic failure.
Observation:
- Quantitative real-time PCR (TaqMan chemistry) was used to measure GBV-C RNA levels in three fulminant hepatitis patients.
- Serum GBV-C RNA levels mirrored alanine aminotransferase (ALT) levels, indicating active viral replication.
- Viral sequencing confirmed persistent infection with the same GBV-C strain throughout the clinical course, even with plasma exchange.
Findings:
- GBV-C RNA was detected and quantified in patients with fulminant hepatitis.
- A strong correlation was observed between viral load and liver injury markers.
- Sequence analysis confirmed the etiological role of GBV-C in the observed liver failure.
Implications:
- GB virus C may be an etiological agent contributing to fulminant hepatic failure.
- These findings challenge the notion of GBV-C as a benign, incidental infection in liver disease patients.
- Further research is warranted to elucidate the pathogenic mechanisms of GBV-C in severe hepatitis.
Background/Aims:
Whether GB virus C causes serious liver diseases remains controversial. The aim of the present study was to determine whether there is an etiological relationship between GB virus C and fulminant hepatitis.
Methods:
The level of GB virus C RNA in the sera of three patients with fulminant hepatitis was quantitatively determined using the newly developed real-time detection polymerase chain reaction method, which is based on Taq Man chemistry. The NS 3 region of the viral genome isolated from the sera was sequenced at several time points to confirm whether the same virus was responsible for fulminant hepatitis during the patients' clinical courses.
Results:
The sensitivity of the PCR was comparable to that of nested PCR and a linear relationship between RNA copy number and threshold cycle was observed for 10(1) and 10(6) RNA copies/ml (r = 0.99). The serum level of GB virus C RNA closely paralleled that of ALT in all patients. Sequence analysis of the NS3 region isolated from the patients' sera revealed that the same GB virus C strain infected the patients during their entire clinical courses, despite plasma exchange therapy.
Conclusions:
These observations suggest that GB virus C may be etiologically associated with fulminant hepatic failure, and is not merely an inactive bystander introduced by therapeutic plasma exchange.