Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology · 2005
Hepatitis C virus superinfection in hepatitis B virus chronic carriers: a reciprocal viral interaction and a variable clinical course.
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Sagnelli Evangelista, Coppola Nicola, Marrocco Cecilia, Onofrio Mirella, Sagnelli Caterina, Coviello Giancarlo, Scolastico Carlo, Filippini Pietro
Аннотация
BACKGROUND: The virological and clinical impact of hepatitis C virus (HCV) superinfection in chronic hepatitis B virus (HBV) carriers has been poorly characterized.
OBJECTIVE: To evaluate the viral interaction, clinical presentation and course of the disease in four HBsAg/HBV-DNA positive chronic hepatitis patients who developed acute HCV infection.
STUDY DESIGN: To evaluate clinical, virological and laboratory data for at least 6 months from the onset of acute HCV infection in patients with chronic HBV infection.
RESULTS: Three patients with acute HCV infection had a normal clinical course, but the remaining patient had severe disease with ascites and a marked decrease in prothrombin activity. In all cases, plasma HBV-DNA, which had been detectable prior to the HCV infection, was no longer detectable when the acute HCV infection occurred. The inhibition exerted by HCV on HBV-DNA persisted throughout the follow-up period in three patients, but was temporary in the one patient who experienced an acute exacerbation of chronic HBV infection. HCV-RNA became persistently undetectable in two patients and reduced to low levels in the other two.
CONCLUSIONS: Acute HCV infection in the four HBV chronic carriers was characterized by a reciprocal inhibition of HBV-HCV genomes and, in one case, by a severe course of disease.
OBJECTIVE: To evaluate the viral interaction, clinical presentation and course of the disease in four HBsAg/HBV-DNA positive chronic hepatitis patients who developed acute HCV infection.
STUDY DESIGN: To evaluate clinical, virological and laboratory data for at least 6 months from the onset of acute HCV infection in patients with chronic HBV infection.
RESULTS: Three patients with acute HCV infection had a normal clinical course, but the remaining patient had severe disease with ascites and a marked decrease in prothrombin activity. In all cases, plasma HBV-DNA, which had been detectable prior to the HCV infection, was no longer detectable when the acute HCV infection occurred. The inhibition exerted by HCV on HBV-DNA persisted throughout the follow-up period in three patients, but was temporary in the one patient who experienced an acute exacerbation of chronic HBV infection. HCV-RNA became persistently undetectable in two patients and reduced to low levels in the other two.
CONCLUSIONS: Acute HCV infection in the four HBV chronic carriers was characterized by a reciprocal inhibition of HBV-HCV genomes and, in one case, by a severe course of disease.