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Published on: July 16, 2012
Hepatitis C Virus as a Possible Helper Virus in Human Hepatitis Delta Virus Infection
Maria Grazia Crobu1,2, Paolo Ravanini1, Clotilde Impaloni1
1Laboratory of Molecular Virology, Maggiore della Carità Hospital, 28100 Novara, Italy.
Insights
Hepatitis C virus (HCV) may assist in spreading hepatitis D virus (HDV) transmission, even without hepatitis B virus (HBV). This preliminary study suggests HCV could act as an HDV helper virus in humans.
Area of Science:
- Virology
- Hepatology
- Infectious Diseases
Background:
- Hepatitis C virus (HCV) has been anecdotally linked to hepatitis D virus (HDV) dissemination.
- Previous studies yielded inconclusive results regarding the role of HCV in HDV spread, particularly through hepatitis B virus (HBV)-independent mechanisms.
Purpose of the Study:
- To investigate the potential role of HCV as a helper virus for HDV transmission in HBV-negative individuals.
- To explore complex transmission dynamics between HCV and HDV.
Main Methods:
- Screening of 146 anti-HCV-positive subjects (including HCV/HIV co-infected and prior HCV-cleared individuals) for anti-HDV antibodies (anti-HD).
- Rigorous exclusion of all current or past HBV infection markers.
- Detailed medical history review for identified anti-HDV positive cases and their close contacts.
Main Results:
- One (0.7%) of the screened patients, co-infected with HCV and HIV, tested positive for anti-HDV but negative for HDV-RNA.
- The anti-HDV positive patient's husband, also HCV/HIV co-infected, had a history of HBV exposure.
- Literature review and case analysis suggested a potential role for HCV in facilitating HDV transmission.
Conclusions:
- This preliminary study offers supporting evidence for HCV acting as an HDV helper virus in human transmission.
- Further large-scale prospective studies are required to validate these findings.
- HCV may play a significant role in the dissemination of HDV, independent of HBV.
Abstract:
Previous studies reported that the hepatitis C virus (HCV) could help disseminate the hepatitis D virus (HDV) in vivo through hepatitis B virus (HBV)-unrelated ways, but with essentially inconclusive results. To try to shed light on this still-debated topic, 146 anti-HCV-positive subjects (of whom 91 HCV/HIV co-infected, and 43 with prior HCV eradication) were screened for anti-HDV antibodies (anti-HD), after careful selection for negativity to any serologic or virologic marker of current or past HBV infection. One single HCV/HIV co-infected patient (0.7%) tested highly positive for anti-HD, but with no positive HDV-RNA. Her husband, in turn, was a HCV/HIV co-infected subject with a previous contact with HBV. While conducting a thorough review of the relevant literature, the authors attempted to exhaustively describe the medical history of both the anti-HD-positive patient and her partner, believing it to be the key to dissecting the possible complex mechanisms of HDV transmission from one subject to another, and speculating that in the present case, it may have been HCV itself that behaved as an HDV helper virus. In conclusion, this preliminary research, while needing further validation in large prospective studies, provided some further evidence of a role of HCV in HDV dissemination in humans.

