Hepatitis C Virus Infection in Chronic Hepatitis B Virus Carriers

Fattovich, Giovanna; Tagger, A.; Brollo, L.; Giustina, G.; Pontisso, Patrizia; Realdi, Giuseppe; Alberti, Alfredo; Ruol, A

doi:10.1093/infdis/163.2.400

Cited by 133 publications

(80 citation statements)

References 8 publications

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“…In addition, studies from India have shown a prevalence of HCV of 3%-31.5% in patients with cirrhosis and chronic liver disease (Table 4) [14]. However, clinical studies from southern Europe and the USA have shown a high percentage of HCV infection in patients with cirrhosis [15], which is consistent with our findings.…”

Section: ،٤ ‫ﺍﻟﻌﺪﺩ‬ ‫ﻋﴩ،‬ ‫ﺍﳋﺎﻣﺲ‬ ‫ﺍﳌﺠﻠﺪ‬ ‫ﺍﻟﻌﺎﳌﻴﺔ،‬ ‫ﺍﻟﺼﺤﺔ‬ ‫ﻣﻨsupporting

confidence: 91%

Hepatitis B and C viral infections in chronic liver disease: a population based study in Qatar

Rikabi¹,

Bener²,

Al‐Marri³

et al. 2009

East Mediterr Health J

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We investigated the incidence of hepatitis B (HBV) and C (HCV) virus infection among patients with liver disease in Qatar from 2000 to 2005. The grading and staging of HBV and HCV cases were obtained from pathology reports at the principal reference laboratory for Qatar. Of the 915 liver patients studied, 29.4% had HCV and 2.5% had HBV. The incidence of HBV and HCV infection was greater in non-Qataris than Qatari nationals and in males than females, especially for HCV. Most cases were uncomplicated (89.0%) and had no inflammation (76.4%). The incidence of HCV has been increasing in liver patients in recent years up to a rate of 481 per 1000 patients with liver disease in 2005. Hepatitis B and C viral infections in

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Section: ،٤ ‫ﺍﻟﻌﺪﺩ‬ ‫ﻋﴩ،‬ ‫ﺍﳋﺎﻣﺲ‬ ‫ﺍﳌﺠﻠﺪ‬ ‫ﺍﻟﻌﺎﳌﻴﺔ،‬ ‫ﺍﻟﺼﺤﺔ‬ ‫ﻣﻨsupporting

confidence: 91%

Hepatitis B and C viral infections in chronic liver disease: a population based study in Qatar

Rikabi¹,

Bener²,

Al‐Marri³

et al. 2009

East Mediterr Health J

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“…Clinical observations in HBV endemic areas showed that most of the HBV-HCV dually infected cases have similar HCV RNA levels as in patients with HCV monoinfection but relatively low levels of serum HBV DNA compared with patients with chronic HBV monoinfection [24][25][26][27][28]. In patients with chronic hepatitis B along with HCV superinfection, hepatitis B e antigen (HBeAg) seroconversion and even HBsAg clearance have been documented [29,30].…”

Section: Viral Interactions Between Hbv and Hcv And Their Impact On Tmentioning

confidence: 99%

Dual chronic hepatitis B virus and hepatitis C virus infection

Liu

Chen

2009

Hepatol Int

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Dual hepatitis B virus (HBV) and hepatitis C virus (HCV) infection are common in HBV or HCV endemic areas. However, several clinical and pathogenetic issues remain unresolved. First, clinical and in vitro studies suggest the interactions between two viruses. The dynamics of the interaction in untreated setting versus treated setting and its influence on the long-term outcomes await further studies. A key issue regarding viral interactions is whether modulation of infection occurs in the same dually infected individual hepatocyte of the liver. Clarifying this issue may help to understand the reciprocal interference between HCV and HBV and provide clues for future immunopathogenetic studies. Second, the prevalence and clinical significance of coexisting occult HBV infection in patients with chronic HCV infection need further investigations. Third, combination therapy of peginterferon alfa2a and ribavirin appears to be just as effective and safe for the treatment of hepatitis B surface antigen (HBsAg)-positive patients chronically infected with active chronic hepatitis C as it is in patients with HCV monoinfection. Nevertheless, one-third of dually infected patients with nondetectable serum HBV DNA-level pretreatment developed HBV reactivation posttreatment. How to prevent and treat this reactivation should be clarified. Furthermore, about 10% of the dually infected patients lost HBsAg. Underlying mechanisms await further investigations. Finally, the optimal treatment strategies for dually infected patients with hepatitis B e antigen-positive chronic hepatitis B should be identified in future clinical trials.

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“…The prevalence of HCV infection in patients with HBV infection has been examined in several studies (62)(63)(64)(65). Interestingly, both clinical and animal studies have shown that HCV might exert a viral interference effect that suppresses or terminates the HBV carrier state (66 -70).…”

Section: Hepatitis C Virus (Hcv)mentioning

confidence: 99%

Mechanisms for Inhibition of Hepatitis B Virus Gene Expression and Replication by Hepatitis C Virus Core Protein

Chen¹,

Kao²,

Chen³

et al. 2003

Journal of Biological Chemistry

146

132

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We have demonstrated previously that the core protein of hepatitis C virus (HCV) exhibits suppression activity on gene expression and replication of hepatitis B virus (HBV). Here we further elucidated the suppression mechanism of HCV core protein. We demonstrated that HCV core protein retained the inhibitory effect on HBV gene expression and replication when expressed as part of the full length of HCV polyprotein. Based on the substitution mutational analysis, our results suggested that mutation introduced into the bipartite nuclear localization signal of the HCV core protein resulted in the cytoplasmic localization of core protein but did not affect its suppression ability on HBV gene expression. Mutational studies also indicated that almost all dibasic residue mutations within the N-terminal 101-amino acid segment of the HCV core protein (except Arg 39 -Arg 40 ) impaired the suppression activity on HBV replication but not HBV gene expression. The integrity of Arg residues at positions 101, 113, 114, and 115 was found to be essential for both suppressive effects, whereas the Arg residue at position 104 was important only in the suppression of HBV gene expression. Moreover, our results indicated that the suppression on HBV gene expression was mediated through the direct interaction of HCV core protein with the trans-activator HBx protein, whereas the suppression of HBV replication involved the complex formation between HBV polymerase (pol) and the HCV core protein, resulting in the structural incompetence for the HBV pol to bind the package signal and consequently abolished the formation of the HBV virion. Altogether, this study suggests that these two suppression effects on HBV elicited by the HCV core protein likely depend on different structural context but not on nuclear localization of the core protein, and the two effects can be decoupled as revealed by its differential targets (HBx or HBV pol) on these two processes of the HBV life cycle.

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Hepatitis C Virus Infection in Chronic Hepatitis B Virus Carriers

Cited by 133 publications

References 8 publications

Hepatitis B and C viral infections in chronic liver disease: a population based study in Qatar

Hepatitis B and C viral infections in chronic liver disease: a population based study in Qatar

Dual chronic hepatitis B virus and hepatitis C virus infection

Mechanisms for Inhibition of Hepatitis B Virus Gene Expression and Replication by Hepatitis C Virus Core Protein

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