Acute hepatitis C virus (HCV) infection in chronic carriers of hepatitis B virus (HBV): the impact of underlying active HBV replication on persistence of HCV infection and antibody responses to HCV

Abstract

Gut 2002;51:95-99 Background and aims: The aim of this study was to assess whether underlying chronic hepatitis B virus (HBV) infection interferes with persistence of hepatitis C virus (HCV) infection and humoral immune responses to HCV in acute HCV infection. Methods: Serial sera from 12 patients with acute HCV infection (group A) and 12 hepatitis B surface antigen (HBsAg) carriers with acute HCV infection (seven anti-hepatitis B e antigen (anti-HBe) positive (group B1) and five hepatitis B e antigen (HBeAg) positive (group B2)) were tested for HCV RNA by polymerase chain reaction, and anti-HCV by third generation enzyme immunoassay and confirmatory assay. Serial serum samples from HBsAg carriers were also tested for HBeAg, anti-HBe, and HBV DNA by hybridisation assay. Results: Persistent HCV viraemia for more than six months was significantly more frequent in groups A (83%) and B1 (86%) than in group B2 (0%). Anti-HCV was detected in 100% and 86% of group A and group B1 one month after onset while only one group B2 patient was transiently anti-HCV positive 1-2 months after onset. Of the latter, three had anti-core 1 less than two months after onset while no patient responded to other HCV antigens. Overall, of six HBsAg carriers with acute self limiting HCV infection, only one had transient anti-HCV and three had transient anti-core 1. HBV DNA became undetectable transiently in four and persistently in one group B2 patient. Conclusion: The presence of active HBV replication can inhibit the persistence of HCV infection and antibody responses to HCV. Acute HCV infection in HBsAg carriers with active HBV replication usually presents transient HCV viraemia with poor antibody responses to HCV.

Clinical Features and Outcome of Chronic Viral Hepatitis with Acute Exacerbation in Patients with Concurrent Infections of Hepatitis B and C Virus

“…Clinical features and outcomes of patients with acute hepatitis related to concurrent HBV and HCV infection, according to HBV DNA positivity genotype type 1b HCV, in contrast to previous studies[13,16,18] that determined that >70% of patients had the genotype 1b. Further studies with a large series of patients are warranted to elucidate this observation.Like other reports…”

“…Studies have determined that concurrent HBV and HCV infection may be associated with a fulminant course of acute hepatitis, with severe forms of chronic liver disease and rapid progression [13][14][15][16][17][18]. Very little is known about the role and course of chronic hepatitis with acute exacerbation in patients with concurrent HBV and HCV infections.…”

“…Some studies have indicated that HCV can inhibit HBV replication or expression [2][3][4][5][6][7][8][9][10][11]. Conversely, HBV inhibiting HCV activities has also been reported [12,13].…”

Hepatitis C virus superinfection in hepatitis B virus chronic carriers: A reciprocal viral interaction and a variable clinical course

“…When HBV acute superinfection occurred in HCV chronic carriers, acute HBV replication strongly inhibited the HCV genome and, compared with acute hepatitis B alone, was associated with a more severe clinical presentation (Sagnelli et al, 2002). HCV superinfection in hepatitis B surface antigen (HBsAg) chronic carriers has been poorly investigated (Romano et al, 1995;Chu et al, 1999a;Chu et al, 2002). We recently followed-up 39 consecutive patients with acute HCV infection documented by seroconversion to anti-HCV.…”

Hepatitis B virus and hepatitis C virus interaction in Huh-7 cells

“…In this respect occult HBV infection, in particular, is often associated with accelerated progression of liver disease in HCV infected individuals [5]. While clinical studies have indicated that HCV dominates over HBV in co-infected individuals 0168 [6][7][8][9], it has also been reported that active replication of HBV can suppress the replication of HCV [10][11][12].…”