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Detection of Low Copy Number Integrated Viral DNA Formed by In Vitro Hepatitis B Infection
Published on: November 7, 2018
Virological profiles in patients with chronic hepatitis C and overt or occult HBV infection
Giovanni Squadrito1, Maria Elena Orlando, Teresa Pollicino
1Dipartimento di Medicina Interna, Università di Messina, Italy.
Insights
Hepatitis B and C virus (HBV and HCV) coinfection shows diverse virological patterns. HCV core gene variability does not influence HBV activity in coinfected patients.
Area of Science:
- Hepatology
- Virology
- Infectious Diseases
Background:
- Hepatitis B virus (HBV) and Hepatitis C virus (HCV) coinfection profiles are not fully understood.
- Occult HBV infection can occur in HBsAg-negative patients with chronic HCV.
- HCV core protein may inhibit HBV replication in vitro.
Purpose of the Study:
- To investigate HBV and HCV virological profiles in coinfection.
- To assess the relationship between HCV core gene variability and HBV activity.
Main Methods:
- Examined 82 anti-HCV positive patients (HBsAg positive, HBsAg negative with occult HBV, HBV negative).
- Evaluated HBV and HCV viremia levels.
- Sequenced the HCV core gene (amino acid sequence 99-116 and entire gene).
Main Results:
- Diverse virological patterns observed in coinfection.
- HCV viremia levels were similar across groups.
- HCV core gene showed high preservation; no link to HBV activity found.
Conclusions:
- Coinfection with HCV and HBV presents a wide range of virological patterns.
- HCV core gene variability is not associated with HBV activity in vivo.
Objectives:
The virological profiles of hepatitis B and C viruses (HBV and HCV) and their interplay in cases of coinfection are undefined. A suppressed and occult HBV infection may occur in hepatitis B surface antigen (HBsAg) negative patients with chronic hepatitis C. The HCV core protein is able to inhibit HBV "in vitro," and serines at positions 99 and 116 are essential for such inhibition. We aimed to assess the HBV and HCV virological profiles in cases of coinfection and to evaluate the relationship between HCV core gene variability and HBV activity.
Methods:
Eighty-two anti-HCV positive patients were examined: 35 cases were HBsAg positive, 24 were HBsAg negative with "occult" HBV infection, and 23 were HBV negative. HBV and HCV viremia levels were evaluated in all cases. HCV genomic region coding for the aminoacid sequence 99-116 of core protein was amplified and sequenced in all HCV RNA positive cases. The entire core gene was amplified and sequenced in three randomly selected cases.
Results:
Serum HCV RNA was detected in all cases but 13, all HBsAg positive individuals; HCV viremia levels of the other 22 HBsAg positive subjects were similar to those detected in HBsAg negative patients with or without occult HBV infection. Among the 35 HBsAg positive patients both HBV DNA and HCV RNA were detected in five cases, HCV RNA alone in 17, and HBV DNA alone in six, whereas seven cases had undetectable levels of both viruses. Sequencing analyses showed that the HCV core gene was highly preserved in all patients.
Conclusion:
A wide spectrum of HCV and HBV virological patterns may occur in a case of coinfection. HCV core variability is not related to HBV activity "in vivo."
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