The prevalence of hepatitis delta virus infection in acute and chronic liver diseases in Turkey: an analysis of clinical studies.

BACKGROUND/AIMS: The objective of this study was to review the studies on hepatitis D virus-related liver diseases and to evaluate the national and regional outcomes in order to identify the hepatitis D virus infection in Turkey. METHODS: This retrospective study included 2182 acute viral hepatitis, 6613 inactive HBsAg carriers, 5961 chronic hepatitis B, 1264 liver cirrhosis and 748 hepatocellular carcinoma cases, who were evaluated for anti-hepatitis D virus positivity at several centers in Turkey since 1980's. ELISA method was used and the results were statistically evaluated. RESULTS: The anti-hepatitis D virus positivity was 3.0% in 1416 acute viral hepatitis and 8.1% in 766 acute hepatitis B cases. This ratio was significantly higher in Diyarbakir than in Istanbul and Ankara for acute viral hepatitis (p<0.001). The mean anti-hepatitis D virus was 4.9% in inactive HBsAg carriers and significantly decreased from 1980 to 2005 (4.1% and 2.9%, respectively p<0.001). The anti- hepatitis D virus was 20% in chronic hepatitis B and 32.5% in liver cirrhosis cases. The positivity were significantly lower in Istanbul and Izmir compared to Diyarbakr and Van (p<0.001). Antihepatitis D virus positivity was decreased in all regions for the last two decades (p<0.001). The rates decreased from 31% to 11% for chronic hepatitis B and from 43.3% to 24% for liver cirrhosis (p<0.001). The mean anti-hepatitis D virus was 23% in hepatocellular carcinoma cases, which was significantly lower in Istanbul and Izmir compared to Diyarbakr and Elaz currency (p<0.0001). CONCLUSIONS: The hepatitis D virus infection is a critical problem in our country, particularly in the Eastern and Southeastern Anatolia. In recent years, the hepatitis D virus infection is decreasing countrywise, however the rate still remains to be critical.     

A retrospective study of the role of delta agent infection in children with HBsAg-positive chronic hepatitis

The prevalence of intrahepatic delta antigen and/or anti-delta antibody was retrospectively investigated in 102 children with chronic HBsAg-positive hepatitis who were seen consecutively in three medical institutions between 1974 and 1982. Delta infection markers were found in 13 patients (12.7%) who exhibited high serum titers of anti-delta antibody; intrahepatic delta antigen was detected in ten. Eleven of the 13 children had severe progressive liver disease associated in all but one with absence of hepatitis B virus replication as evaluated by analysis of serum hepatitis B virus DNA. The factors which seem to increase the risk of delta infection in children who are hepatitis B virus carriers are geographic origin, a history of exposure to blood derivatives and age. A further 37 of 102 children had chronic active hepatitis (20 patients) or cirrhosis (17 patients) without evidence of delta infection. These results indicate that delta infection occurs in children with chronic hepatitis. This possibility should be considered in investigation of children with HBsAg-positive chronic liver disease. Although the delta agent is an important cause of progressive liver disease in children who are chronic HBsAg carriers, severe liver injury and especially cirrhosis can occur without evidence of delta infection.     

Hepatitis B virus replication in patients with chronic liver diseases

One hundred and seventy five subjects with chronic liver diseases which included patients with chronic active hepatitis (90), liver cirrhosis (31) and asymptomatic hepatitis B carriers (54), were included in the study. Hepatitis B virus (HBV) specific DNA-polymerase activity and HBe-markers were tested as markers of HBV-multiplication. In HBsAg positive samples, DNA-P activity was positive in 44.4% of the HBV carriers, 52.9% of the patients with chronic active hepatitis and 81.8% of the patients with liver cirrhosis. The corresponding figures for the presence of HBeAg in these groups were 18.5, 26.5 and 45.5% respectively. Virus multiplication was also observed in 41.1 and 44.4% patients with chronic active hepatitis and liver cirrhosis respectively, in the absence of HBsAg. The results of the present study show that hepatitis B virus is the most important etiological factor of chronic liver diseases in India. Most of our patients of chronic liver diseases seems to have contacted HBV infection as young adults and the mode of transmission is likely to be horizontal rather than vertical. The virus replicating markers correlate well with the severity of the liver injury and decreased with the age. DNA-P activity is a more sensitive marker of viral multiplication than HBeAg. Viral multiplication was also found to occur in the absence of the usual HBV markers. Continued viral multiplication in patients with chronic active hepatitis and liver cirrhosis is implicated in continued liver injury and progressive liver disease.     

Hepatitis B virus DNA in chronic HBsAg carriers: correlation with HBeAg/anti-HBe status, anti-HD and liver histology.

Hepatitis B virus DNA was determined in the sera of 198 chronic hepatitis B surface antigen (HBsAg) carriers by the spot hybridization technique. The results were correlated with hepatitis Be antigen (HBeAg) and antibody (anti-HBe), delta antibody (anti-HD) and liver histology. All subjects had a liver biopsy. The prevalence of HBV DNA was 63% in HBeAg-positive subjects and 8.8% in anti-HBe positives. HBV DNA was not found more frequently in chronic HBsAg carriers who had histological evidence of liver disease than in carriers without such evidence. Anti-HD was detected in 48.5% of subjects, with an increasing trend (p less than 0.001) according to the severity of liver disease. Among patients with more severe liver disease (CAH and cirrhosis), HBV DNA and HBeAg were detected less frequently in anti-HD-positive than in anti-HD-negative subjects (7% vs. 42.3%, p less than 0.001 and 7% vs. 34.4%, p less than 0.005, respectively). These findings indicate that HDV infection jointly affects both HBeAg status and HBV DNA.     

Delta agent infection in acute hepatitis and chronic HBsAg carriers with and without liver disease

Hepatitis B virus (HBV) is a major cause of chronic liver disease in southern Italy. In the same area superinfection with the delta agent is endemic. To assess the prevalence of delta infection in a large population of patients with acute and chronic HBV related liver disease and to look for differential features among delta infected and uninfected subjects sera from 592 consecutive HBsAg positive patients were tested for the delta/anti-delta system by RIA. In no case was delta Ag found in serum. The prevalence of anti-delta was low in acute hepatitis (6.6%) and in asymptomatic carriers (6.4%) but raised in chronic active hepatitis with or without cirrhosis (52.3%). A decrease in frequency of anti-delta was seen in inactive cirrhosis (38.8%) and in hepatocellular carcinoma (11.9%). A younger mean age of delta-infected subjects was observed in each type of chronic liver disease. Our data confirm that delta agent superinfection is definitely associated with severe chronic active liver disease. The difference in age between anti-delta positive and negative patients suggests that delta infection accelerates the natural history of HBV related liver disease.     

A Case Report of Hepatocellular Carcinoma 5 Years After HBsAg Loss in Chronic Hepatitis Delta: How Long Surveillance is Required?

BackgroundHepatitis delta virus infection occurs as acute coinfection or as superinfection in patients with preexisting chronic hepatitis B. Chronic hepatitis delta leads to more severe disease than chronic hepatitis B, with more rapid progression of fibrosis and increased risk of hepatocelullar carcinoma.Case reportWe report a case of hepatocelullar carcinoma 5 years after spontaneous clearance of Hepatitis B surface antigen in a patient with previous chronic hepatitis delta. He had been diagnosed with acute hepatitis delta superinfection 30 years ago which evolved to chronic delta infection and subsequently development of liver cirrhosis. Despite no specific antiviral treatment, he lost HBsAg persistently with later regression of cirrhosis.ConclusionsIn patients with cirrhosis due to chronic hepatitis delta who cleared HBsAg with improvement of liver fibrosis by non invasive techniques, it remains unknown how long hepatocelullar carcinoma surveillance has to be maintained.     

Prognosis following spontaneous HBsAg seroclearance in chronic hepatitis B patients with or without concurrent infection

BACKGROUND & AIMS: Spontaneous hepatitis B surface antigen (HBsAg) seroclearance is a rare event in patients with chronic hepatitis B virus infection. The aim of this study was to clarify the controversy on long-term prognosis following spontaneous HBsAg seroclearance using a large series of patients. METHODS: A total of 218 patients (172 men and 46 women) who had undergone spontaneous HBsAg seroclearance were followed up for 12-179 months (median, 61.7 months; mean, 63.4 +/- 38.5 months) with liver biochemistry, serology, measurement of alpha-fetoprotein level, and abdominal ultrasonography every 6 months or every 3 months for the 29 patients who had developed cirrhosis at the time of HBsAg seroclearance. RESULTS: Of the 189 patients who were noncirrhotic at the time of HBsAg clearance, 3 (1.6%) developed cirrhosis, 2 (1.1%) developed hepatocellular carcinoma (HCC), and 1 died of HCC. These complications all developed in patients with concurrent hepatitis C virus or hepatitis delta virus infection (P < 0.001). The prognosis of the noncirrhotic patients without concurrent infection was significantly better than that of the matched control group (elevation of alanine aminotransferase level, 11.6% vs. 0%, P < 0.001; development of cirrhosis/HCC, 4% vs. 0%, P = 0.004). In contrast, of the 29 patients who had developed liver cirrhosis, 4 (13.8%) had hepatic decompensation and one died of HCC. CONCLUSIONS: The prognosis following spontaneous HBsAg seroclearance is excellent, except in patients with cirrhosis or those with concurrent hepatitis C virus or hepatitis delta virus infection.     

Delta infection in chronic HBs Ag carriers in Tunisia: high prevalence in chronic asymptomatic HBs Ag carriers and in HBs Ag positive cirrhosis

The presence of hepatitis B virus DNA, delta antigen and anti-delta antibodies was examined in 159 Tunisian chronic HBs Ag carriers: 45 were asymptomatic and 114 suffered from cirrhosis. Serum hepatitis B virus DNA was detected in two (4.5%) asymptomatic HBs Ag carriers and in 11 (10%) HBs Ag positive cirrhosis patients. The prevalence of HDV infection determined by the presence of anti-delta was relatively high in asymptomatic HBs Ag carriers (33%) and in HBs Ag positive cirrhosis patients (21%). Active ongoing HDV infection, detected by serum HD Ag and anti-delta IgM, was shown in five patients with cirrhosis and active hepatitis B virus replication. We conclude that hepatitis delta virus may be endemic in Tunisia and does not always inhibit hepatitis B virus replication.     

Infection with hepatitis delta virus in patients with fulminant hepatitis B and chronic HBsAg carriers in Bulgaria

To evaluate the prevalence and clinical significance of delta infection in a Bulgarian population, 105 HBsAG positive patients with chronic liver diseases, and 42 patients who had died of fulminant hepatitis B were studied. Delta antigen was detected by direct immunofluorescence in the liver of 9 patients with chronic HBV infection (8.6%), and in 3 patients with fulminant hepatitis (7.14%). All chronic HBsAg carriers with delta superinfection had chronic active hepatitis or active liver cirrhosis. They were predominantly anti-HBe (+) in the serum. The mean age and the mean values of serum transaminase did not differ in delta antigen positive and negative patients with chronic liver diseases. A history of parenteral manipulations directly before the hepatitis was present in patients with delta antigen positive fulminant hepatitis. These results indicate a relatively low incidence of delta infection in our population, but it is invariably associated with severe liver disease.     

Delta hepatitis in Lebanon. Prevalence studies and a report on six siblings with chronic delta-positive active hepatitis

The prevalence of delta infection in Lebanon is reported for the first time. Delta antigen and antibody were screened for in serum of 43 patients consecutively seen in hospital, 22 with acute hepatitis B (anti-HBc IgM-positive), and 21 with histological evidence of chronic active hepatitis, 6 of whom were brothers in a sibship of eleven. Twenty asymptomatic HBsAg carriers without clinical or biochemical evidence of liver disease were similarly studied. None of the asymptomatic carriers or acute hepatitis B patients had markers of delta infection. In contrast, delta antibody in high titre (greater than 1:5000) was found in 12 (57%) of the patients with chronic active hepatitis, including all six brothers. Five sisters in the sibship were anti-HBs-positive without evidence of liver disease, suggesting a horizontal mode of transmission of the delta virus, as a superinfection on a hepatitis B carrier state. Excluding the sibship, delta infection was present in 6 of 15 (40%) chronic active hepatitis patients. This prevalence is similar to other Middle Eastern countries. Delta infection was associated with severe liver disease.     

Prospects for hepatitis B virus eradication and control of hepatocellular carcinoma

Hepatitis B virus infection is the most common cause of chronic hepatitis, liver cirrhosis and hepatocellular carcinoma worldwide. In areas hyperendemic for HBV infection, the related complications occur mostly during adulthood. However, nearly half of all primary infection in chronic carriers occurs in the perinatal period through maternal transmission, the other half arising from horizontal transmission mainly through intrafamilial spread or injection using unsterilized needles. A universal vaccination programme is better than immunization for at-risk groups. Hepatitis B vaccination should be integrated into the Expanded Programme on Immunization in children. Universal immunization against hepatitis B virus has proved to be effective in reducing the hepatitis B carrier rate to one-tenth of the prevalence before the vaccination programme in highly endemic areas, and the incidence of hepatocellular carcinoma in children has also been shown to be significantly reduced. Continued efforts to implement universal vaccination programmes worldwide will very likely reduce the incidence of hepatitis B virus-related diseases, particularly liver cirrhosis and hepatocellular carcinoma.     

Hepatitis B virus genotypes and clinical manifestation among hepatitis B carriers in Thailand

BACKGROUND: Hepatitis B virus (HBV) genotypes have distinct geographic distributions. The aim of the present study was to evaluate the distribution of HBV genotypes and their clinical relevance in Thailand. METHODS: Hepatitis B virus genotypes among 107 hepatitis B carriers residing in Thailand were evaluated using serologic and genetic methods. They were clinically classified into asymptomatic carriers with normal serum alanine transaminase (ALT) levels and patients with chronic liver disease, such as those with chronic hepatitis (CH), liver cirrhosis (LC) and hepatocellular carcinoma (HCC). RESULTS: Hepatitis B virus genotype distribution among the 107 patients was 25.2% for genotype B, 72.0% for genotype C and 2.8% for genotype D. The serum ALT levels, HBV-DNA and hepatitis B e antigen positivity were significantly higher in carriers infected with genotype C HBV than in those infected with genotype B (P < 0.05). The proportion of genotype B HBV was higher in asymptomatic carriers than in patients with CH and those who developed liver disease, such as LC and HCC (45.5, 16.9 and 25.0%, respectively; P < 0.05). In contrast, the proportion of genotype C HBV was higher in patients who developed liver disease and CH than in asymptomatic carriers (68.7, 83.0 and 50.0%, respectively; P < 0.05). Phylogenetic analysis based on entire genome sequences revealed three HBV isolates, which were classified into a subgroup of genotype C in isolates from South-East Asian countries. CONCLUSIONS: Genotypes B and C are the predominant types among hepatitis B carriers residing in Thailand and those genotypes influence the clinical manifestation in carriers with chronic hepatitis B infection.     

Long-term follow-up of anti-HBe-positive chronic active hepatitis B

Twenty-eight patients with chronic active hepatitis without cirrhosis who were positive for hepatitis B surface antigen and antibody to hepatitis B e antigen were followed for 1 to 15 years (mean 6.6 years) and underwent follow-up biopsy. At presentation, 12 of the 28 patients (43%) had hepatitis B virus DNA in serum, 10 (36%) had serologic evidence of hepatitis delta virus infection and 6 (21%) had no serologic markers of either hepatitis B virus replication or hepatitis delta virus infection. During follow-up, 15 (54%) patients developed active cirrhosis, including eight patients with hepatitis delta virus infection and five with hepatitis B virus DNA in serum. In seven (47%) of the 15 patients, cirrhosis developed within the first 2 years; all seven patients had bridging necrosis in the first liver biopsy, and five of these were infected with hepatitis delta virus. The remaining 13 (46%) patients did not develop cirrhosis during follow-up and showed either unchanged features of chronic active hepatitis (seven cases) or histologic improvement to chronic persistent hepatitis (five cases) or to normal liver (one case). In conclusion, the prognosis of anti-HBe-positive patients with chronic hepatitis B is poor, as 54% of the cases developed cirrhosis during a mean histologic follow-up period of 4.5 years, mainly in association with hepatitis delta virus infection or continuing hepatitis B virus replication.     

Anti-hepatitis A virus seroprevalence among patients with chronic viral liver disease in Korea

BACKGROUND/OBJECTIVE: It is generally recommended that patients with chronic viral hepatitis should be vaccinated against hepatitis A virus (HAV) infection. We intended to evaluate the prevalence of IgG anti-HAV according to age in patients chronically infected with hepatitis B virus or hepatitis C virus in Korea. METHODS: From June to October 2006, 303 patients (226 male, 77 female) with chronic hepatitis, liver cirrhosis, or hepatocellular carcinoma were recruited (mean age 50.8+/-14.4 years; range 16-84). The sera were tested for antibodies to HAV, and overall and age-specific seroprevalence of anti-HAV was assessed. RESULTS: Hepatitis B virus infection was the etiology of liver diseases in 267 patients (88.1%), with hepatitis C virus infection in 36 (11.9%). The distribution of clinical diagnosis was chronic hepatitis in 86 patients (28.4%), liver cirrhosis in 36 (11.9%), and hepatocellular carcinoma in 181 (57.9%). The patients were categorized by decade of age and the distribution was as follows: nine patients (2.5%) in their teens, 23 (6.2%) in their 20s, 36 (12.4%) in their 30s, 78 (25.7%) in their 40s, 72 (24.1%) in their 50s, and 85 (29%) >or=61 years. The overall seroprevalence of anti-HAV was 87.8% (266/303), and no difference was observed in sex (86.7 vs. 90.9%, P=0.42). The seroprevalence in each age group was 22.2, 26.1, 72.2, 97.4, 100 and 98.8%, respectively, showing marked increase in those over 40 years of age (P<0.001). CONCLUSION: Our study demonstrates that most Korean patients over 40 years of age with chronic liver disease have already been exposed to HAV.     

Relationship between levels of DNA damage in lymphocytes and histopathological severity of chronic hepatitis C and various clinical forms of hepatitis B

BACKGROUND AND AIM: A significant proportion of cancer is attributable to DNA damage caused by chronic infection and inflammation. Because both hepatitis B and C viruses (HBV and HCV, respectively) cause chronic infection and inflammatory disease, the aim of the present study was to investigate whether there is a difference in peripheral DNA damage in patients with chronic HCV compared with patients with chronic HBV; and whether there is an association in the level of peripheral DNA damage with a natural history of HBV infection. METHODS: Twenty patients with chronic hepatitis C, 20 patients with chronic hepatitis B, 11 patients with cirrhosis secondary to hepatitis B, 12 inactive hepatitis B s antigen (HBsAg) carriers and 21 healthy subjects were included in the study. The DNA damage in lymphocytes was determined using the alkaline comet assay. RESULTS: Although the chronic hepatitis C group had similar levels of DNA damage compared with patients with cirrhosis due to hepatitis B (P > 0.05) and non-cirrhotic patients with chronic hepatitis B (P > 0.05), they had higher levels of DNA damage compared with inactive HBsAg carriers (P = 0.021) and controls (P = 0.001). Hepatitis B cirrhotic patients and patients with chronic hepatitis B had significantly higher levels of DNA damage than inactive HBsAg carriers (P = 0.002 and P = 0.012, respectively) and controls (both P = 0.001). Linear logistic regression analysis showed that chronic hepatitis C and HBV-related cirrhosis were discriminators in determining DNA damage in lymphocytes (beta 0.424 and P = 0.013, beta 0.393 and P = 0.016, respectively). CONCLUSIONS: Chronic hepatitis C, based on the severity of liver disease, or cirrhosis as an advanced form of HBV infection increase DNA damage in lymphocytes independently of confounding factors such as age, gender, body mass index and smoking habits.     

Correlations between hepatitis B virus genotype and cirrhotic or non-cirrhotic hepatoma

BACKGROUND/AIMS: Hepatoma arising in cirrhotic and non-cirrhotic livers might have different virological and clinical factors in hepatitis B virus carriers. This study was performed to elucidate the correlation between hepatitis B virus genotypes and clinical characteristics of patients with cirrhotic and non-cirrhotic hepatoma. METHODOLOGY: One hundred and fifty-five hepatitis B virus carriers who received hepatic resection for hepatoma were investigated to determine hepatitis B virus genotypes and clinical features. RESULTS: Of 155 patients, 84 were genotype B infection, and 67 genotype C. Compared to genotype C carriers, genotype B analogs had a significantly lower rate of liver cirrhosis (p=0.005), lower hepatitis B e antigen positive rates (p=0.0008), and lower fibrosis scores (p=0.003). In comparison to cirrhotic hepatoma patients, non-cirrhotic counterparts were younger (p=0.041), had a higher platelet count (p<0.001), lower hepatitis B e antigen positive rates (p=0.023), predominantly genotype B (p=0.005), lower inflammation scores (p<0.001). Using multivariate analysis, non-cirrhotic hepatoma was associated with genotype B infection (OR=2.85, 95% CI=1.44-5.64) and younger age (OR=0.967, 95% CI=0.94-0.99) in hepatitis B virus carriers. CONCLUSIONS: Our study suggested that hepatitis B virus genotype B infection might be an important factor for non-cirrhotic hepatoma.     

Hepatitis E virus is responsible for decompensation of chronic liver disease in an endemic region.

BACKGROUND: Hepatitis A virus infection in patients with previously stable chronic liver disease is associated with liver decompensation. Whether infection with hepatitis E virus (HEV) also does so is not known. METHODS: We studied 32 patients with decompensated liver disease and definite evidence of underlying cirrhosis for evidence of recent HEV infection. RESULTS: Of 32 patients, 14 (44%) had detectable IgM anti-HEV in their serum. In comparison, only 3 of 48 (6%) patients with stable cirrhosis and no recent decompensation had such antibodies (p<0.0001). Of the 14 patients with evidence of recent HEV infection, 11 had history of prodrome. The etiology of cirrhosis in these patients was: hepatitis B 6, hepatitis C 2, both hepatitis B and C 2, Wilson's disease 1, autoimmune 1 and cryptogenic 2. Two of these 14 patients died. Twelve patients survived, as compared to 9 of 18 patients without evidence of recent HEV infection (p<0.01). CONCLUSION: HEV infection is a frequent cause of decompensation in patients with liver cirrhosis in HEV-endemic regions.     

Delta hepatitis in the Los Angeles area: a report of 126 cases

We describe the clinical course in 126 patients with delta hepatitis who have been evaluated in Los Angeles since 1967. In approximately two thirds of all patients, delta infection was associated with chronic hepatitis B. Most patients were members of two major risk groups: 65.9% were intravenous drug abusers, 11.9% were male homosexuals, and another 9.5% were both intravenous drug users and male homosexuals. The overall case fatality rate was 23%; fulminant hepatitis caused 17 of 29 (59%) deaths. Advanced liver disease occurred significantly more frequently in patients who had established chronic delta infections than in hepatitis B virus carriers with recent delta superinfections. Nonfatal infections with both hepatitis B virus and delta hepatitis virus resulted in clearance of both agents, whereas superinfection in carriers of chronic hepatitis B virus usually led to chronic delta hepatitis. Spontaneous loss of chronic delta infection was not observed. Delta hepatitis, a longstanding infection seen in patients in the Los Angeles area, has caused fulminant hepatitis and progressive liver disease in both intravenous drug users and male homosexuals.     

High prevalence, low pathogenicity in hepatitis G virus in kidney transplant recipients

BACKGROUND: Prevalence and pathogenicity of hepatitis G virus infection in long-term renal transplant recipients, are not fully known. AIM: To evaluate long-term impact of HGV infection on liver disease of renal transplanted patients. PATIENTS AND METHODS: A total of 155 hepatitis B surface antigen negative kidney transplant recipients, followed for a mean of 11 years after renal transplantation, were studied. Of these 48 (31%) patients had persistently elevated serum aminotransferase values. Frozen serum samples were tested for HGV-RNA and HCV-RNA by nested reverse transcribed polymerase chain reaction, and for anti-hepatitis G virus and anti-hepatitis C virus by enzyme-linked immunosorbent assay Hepatitis C virus-RNA was typed by a line probe assay and quantified by a branched DNA signal amplification assay RESULTS: Hepatitis G virus-RNA was detected in 37 (24%) patients and anti-hepatitis G virus in another 26 (17%). Seventy (45%) patients had serum anti-hepatitis C virus and 63 of these (90%) had serum hepatitis C virus-RNA. Hepatitis G virus-RNA positive and negative patients were similar in terms of age, sex, duration of dialysis, rate of transfusion, chronic liver disease, rate of hepatitis C virus infection and immunosuppressive therapy. Fifteen (41%) hepatitis G virus-RNA seropositive patients were hepatitis C virus co-infected. Hepatitis C virus-RNA levels were significantly lower in the 15 hepatitis C virus/hepatitis G virus co-infected patients than in the 48 patients with hepatitis C virus infection only (2.2 vs 10.8 MEq/ml, p = 0.02). Only 3 hepatitis G virus carriers had persistently elevated alanine aminotransferase compared to 29 hepatitis C virus carriers (14% vs 60%, p < 0.001), 10 patients co-infected with both hepatitis G virus and hepatitis C virus, and in 6 patients with neither infection (67% vs 8%, p < 0.001). CONCLUSIONS: Hepatitis G virus infection is common among kidney transplant patients, it carries a low risk of chronic liver disease even in long-term follow-up. Low levels of hepatitis C virus-RNA found in hepatitis G virus carriers suggest an interaction between these two viruses in immunosuppressed patients.