GB virus-C/hepatitis G virus infection in an area endemic for viral hepatitis, chronic liver disease, and liver cancer

Kao, Jia‐Horng; Pj, Chen; My, Lai; Chen, W; Liu, Ding-Ping; Wang, Jann-Tay; Mc, Shen; Ds, Chen

doi:10.1016/s0016-5085(97)70139-2

Cited by 74 publications

(61 citation statements)

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“…Although the percentage of chronic active hepatitis was higher in patients with double infection, the cirrhosis was signi®cantly more prevalent in patients infected with HCV alone. On the whole, these data indicate that GBV-C/HGV does not determine a CLD, in line with the results obtained by other groups (Kao et al, 1997). Interestingly, none of the positive four cases, besides the blood donors, had a history of blood transfusion or exposure to several risks (i.v.…”

Section: Controlssupporting

confidence: 89%

GBV‐C/HGV and HCV infection in mixed cryoglobulinaemia

Crovatto¹,

Mazzaro²,

Mishiro

et al. 1999

Br J Haematol

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Summary. Recently, a new, suspected hepatotropic virus has been identi®ed. Named GBV-C/HGV, this virus shares with the hepatitis C virus (HCV) routes of transmission and molecular organization. Indeed, a proportion of HCVinfected patients (10±25%) are also carriers of GBV-C/HGV. Since mixed cryoglobulinaemia (MC) is closely associated with HCV infection, the aim of this study was to determine the prevalence of GBV-C/HGV infection in MC patients, and to investigate whether the double infection in¯uenced the clinical and/or laboratory aspects of the disease.52 patients affected by MC were studied. 100 patients affected by HCV-positive chronic liver disease (CLD) without MC were used as control group. To determine the prevalence of GBV-C/HGV infection in general population, 150 blood donors were studied, as well as 80 patients affected by non-A±E CLD.Among the MC patients, only ®ve (9´6%) were positive for both HCV and GBV-C/HGV infection. No difference was found between patients with and without double infection as regards main clinical and laboratory aspects. Among HCVpositive CLD cases, 27 were positive for double infection. Among blood donors, the prevalence of GBV-C/HGV infection was 8´0%, whereas in cases with cryptogenetic CLD the prevalence was 5´0%.In conclusion, these data show that GBV-C/HGV infection does not play any role in the pathogenesis of MC.

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Section: Controlssupporting

confidence: 89%

GBV‐C/HGV and HCV infection in mixed cryoglobulinaemia

Crovatto¹,

Mazzaro²,

Mishiro

et al. 1999

Br J Haematol

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“…Nevertheless, by using highly sensitive PCR assays (Table 1), we found that the prevalences of occult HBV infection were comparable in patients with chronic HCV infection (14.8%) and healthy adults (15%), implying that the risk of occult HBV infection among HCV carriers is not increased compared to that for the general population in Taiwan. These findings are not unanticipated because most adults in Taiwan contracted HBV infection during childhood, and superinfection with other viruses including HCV may occur thereafter (8). In addition, the low-level replication of HBV in patients with occult HBV infection does not appear to result from interference by HCV because the occult HBV infection is not necessarily accompanied by HCV infection but is observed at the same rate in healthy controls (17).…”

Section: Discussionmentioning

confidence: 92%

Occult Hepatitis B Virus Infection and Clinical Outcomes of Patients with Chronic Hepatitis C

et al. 2002

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Although occult hepatitis B virus (HBV) infections in individuals without detectable hepatitis B surfaceantigen (HBsAg) may occur and have been reported to be common in patients with chronic hepatitis C, the clinical relevance remains controversial. We searched for serum HBV DNA in 210 HBsAg-negative patients with hepatitis C virus (HCV)-related liver disease (110 patients with chronic hepatitis, 50 patients with cirrhosis, and 50 patients with hepatocellular carcinoma) by PCR. Most of the patients had detectable antibodies to HBsAg or HBV core antigen. All of the 110 chronic hepatitis C patients were treated with a combination therapy consisting of interferon plus ribavirin. In addition, 100 HBsAg-negative healthy adults served as controls. Thirty-one of the 210 patients (14.8%) had HBV DNA in their sera, as did 15 of the 100 healthy controls (15%). HBV DNA was not detected in the sera of those negative for serological markers of HBV infection. In patients with chronic HCV infection, the prevalence of occult HBV infection did not parallel the severity of liver disease (14.5% in patients with chronic hepatitis, 8% in patients with liver cirrhosis, and 22% in patients with hepatocellular carcinoma). In addition, the sustained response to combination therapy against hepatitis C was comparable between patients with and without occult HBV infection (38 versus 39%). In conclusion, these data suggest that occult HBV infection does not have clinical significance in chronic hepatitis C patients residing in areas where HBV infection is endemic.Hepatitis B virus (HBV) and hepatitis C virus (HCV) infections account for a substantial proportion of cases of chronic liver disease including chronic hepatitis, cirrhosis, and liver cancer. It is estimated that there are 350 million HBV carriers and 170 million HCV carriers worldwide (6). HBV and HCV are transmitted parenterally and share common routes of infection; thus, infection with both viruses may occur, particularly in areas where the two viruses are endemic and among people at high risk for parenteral infections (4, 15). The diagnosis of HBV infection is usually based on the detection of hepatitis B surface antigen (HBsAg), and the disappearance of this antigen indicates the clearance of HBV (6). However, previous studies have shown that HBV DNA can be detected in patients with chronic liver disease who are negative for HBsAg but positive for antibodies to hepatitis B core antigen (anti-HBc) (1, 12, 21). More recently, this so-called occult HBV infection has frequently been identified in patients with chronic HCV infection (5,10,19), and in such patients this occult infection may be associated with more severe liver damage and even the development of hepatocellular carcinoma (HCC) (3,18,20). In addition, several studies have suggested that occult HBV infection may correlate with a lack of response to interferon treatment in patients with chronic hepatitis C (3, 5, 22). Taken together, a low-level HBV infection not only may contribute to the severity of HCV-related liver d...

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“…This low incidence is consistent with the reported by Sugai et al [18] that GBV-C/HGV RNA was detected only in 1 of 12 patients with non-B non-C chronic liver disease. Kao et al [19] also reported co-infection with GBV-C/HGV in patients who were positive for hepatitis B or hepatitis C did not cause any alteration in clinical features during follow-up with respect to development of HCC. Taken together with the present findings, involvement of GBV-C/HGV in the pathogenesis of non-B non-C HCC may be unlikely.…”

Section: Discussionmentioning

confidence: 95%