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A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target
Published on: May 10, 2022
[Viral co-infections in hepatitis C: HBV, HBV-C/HGV and TTV studies]
Alajos Pár1, Mária Takács, Judit Brojnás
1Pécsi Tudományegyetem, Altalános Orvostudományi Kar, I. Belgyógyászati Klinika, Pécs.
Insights
Co-infections with hepatitis B virus (HBV), GBV-C (HGV), and TT virus (TTV) do not appear to affect chronic hepatitis C (HCV) progression. However, interferon treatment for HCV showed a potential antiviral effect on TTV.
Area of Science:
- Hepatology
- Virology
- Infectious Diseases
Context:
- Chronic hepatitis C (HCV) is often studied alongside other hepatitis viruses.
- Understanding co-infections is crucial for managing liver disease progression.
- Hepatitis B virus (HBV), GBV-C (HGV), and TT virus (TTV) are relevant co-infecting agents.
Purpose:
- To investigate the prevalence of HBV, HGV, and TTV co-infections in chronic HCV patients and carriers.
- To assess the influence of these co-infections on the clinical course of HCV infection.
- To evaluate the impact of interferon (IFN) therapy on co-infection dynamics.
Summary:
- A study of 110 HCV-positive individuals (77 with chronic hepatitis C, 33 carriers) analyzed co-infections using PCR and ELISA.
- Results showed varying prevalence rates for HBV, HGV, and TTV across patient groups.
- Neither HBV, HGV, nor TTV significantly altered the course of chronic HCV infection.
Impact:
- The findings suggest that HBV, HGV, and TTV do not significantly impact HCV progression.
- Lower TTV detection in sustained IFN responders implies a potential antiviral effect of IFN on TTV.
- This research contributes to understanding the complex interplay of viral hepatitis infections.
Background/Aims:
The prevalence of co-infections with hepatitis B virus (HBV) and novel hepatitis viruses GBV-C (Hepatitis G virus, HGV) and TT virus (TTV) in chronic hepatitis C (HCV) infection has been studied. In patients with chronic hepatitis C and in asymptomatic healthy HCV carriers, the influence of these agents on the course of HCV infection was assessed.
Methods:
a total of 110 HCV-positive individuals, among them 77 patients with chronic hepatitis C--50 of them treated with interferon (IFN)--and 33 HCV carriers with normal alanine aminotransferase have been investigated. HBV-DNA, HGV RNA and TTV DNA were detected by PCR, to determine HBsAg and anti-HBc ELISA technic has been used.
Results:
In the healthy population, the prevalence of anti-HCV was 0.3%, HBsAg 0.09%, anti-HBc 2.5%, HGV RNA 8.0% and TTV DNA 18.5%, respectively. In chronic hepatitis C HBsAg (accompanied with HBV-DNA) occurred in 1.29%, anti-HBc 25.97%, HGV RNA in 9.09% and TTV DNA in 40.25% of cases. In IFN-treated patients with sustained remission, the frequency of TTV was 20% vs. 45.7% found in non-responders. Among asymptomatic HCV-carriers, the prevalence of anti-HBc was 27.27%, HGV RNA 9.09% and TTV DNA 75.7% respectively.
Conclusions:
Neither previous HBV infection, nor HGV RNA and TTV DNA had apparent effect on the course of chronic HCV infection. TTV was detected with the lowest frequency in persons with sustained remission due to IFN, suggesting antiviral effect of IFN on TTV.
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