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All the incubation steps were performed using a shaker

All the incubation steps were performed using a shaker. C virus (HCV) antibody, hepatitis B surface antigen (HBsAg), and hepatitis B core antibody (HBcAB). Twenty five healthy children of matched age & sex were used as controls. Results HGV RNA was positive in 9 (26.5%) of HD and 9 (13.6%) of predialysis children. Anti E2 was positive in 14 (41.2%) of HD and 19 (28.8%) of predialysis children. In comparison to controls; CRF (n = 100); HD and predialysis children had significantly higher prevalence of anti E2 [4% VS 33% for all CRF cases; (p = 0.002)& FTY720 (Fingolimod) 41.2% (p = 0.002) and 28.8% (p = 0.01); for HD and predialysis groups; respectively]. HGV RNA was significantly more prevalent only in HD children in comparison to controls (p = 0.03). FTY720 (Fingolimod) HD and predialysis children did not have significant difference in FTY720 (Fingolimod) the prevalence of HGV RNA (p = 0.16) or anti E2 (p = 0.26). HGV exposure was not correlated with positivity of anti HCV (p = 0.32), HCV RNA (0.09), HBsAg/HBcAB (p = 1), age (p = 0.06), or gender (p = 0.83). It was significantly correlated with duration of the disease (p 0.001). Ongoing HGV infection was significantly more prevalent with frequent blood transfusion (p 0.001). There were no significant differences in serum FTY720 (Fingolimod) levels of ALT (p = 0.09), total bilirubin (p = 0.1) and albumin (p = 0.06) in children with ongoing infection in comparison to healthy controls. Conclusions The frequency of HGV exposure in Egyptian children FTY720 (Fingolimod) with CRF appears to be high and is mainly related to frequent blood transfusions and longer disease duration. HGV infection in these children is not associated with significant changes in hepatic biochemical parameters. Background Infections are one of the important causes of morbidity and mortality in patients with end stage renal failure[1]. Chronic hepatitis is a major complication of chronic haemodialysis (HD). Initially; hepatitis B virus (HBV) infection was the most common etiologic agent of chronic hepatitis in patients on chronic HD. Later; after HBV vaccines became available and measures for screening and exclusion of hepatitis B surface antigen (HBsAg) positive blood were routinely used, HBV infection dropped significantly. Subsequently; however, hepatitis C virus (HCV) emerged as a new problem. In USA; rates of positive anti HCV reached up to 36% in HD patients in 1990s [2]. Two different laboratories in the AKAP13 USA isolated a new flavivirus-like RNA virus in the years 1995 and 1996. The first laboratory named it “G B virus-C (GBV-C)” and the other “hepatitis G virus (HGV)”. Both viruses were subsequently considered different genotypes of the same virus because they were found to share most of the nucleotide and amino acid sequences [3]. Both viruses have a single stranded RNA genome of approximately 9.4 kb. It encodes a single poly protein of 2900 amino acids in which the non structural proteins are located at the C terminal end and the structural proteins at the N terminal end [4]. The HGV genome encodes an open reading frame coding for two envelop proteins (E1 & E2) [5]. The ongoing HGV infection can be diagnosed by demonstration of viremia in patient blood by reverse transcriptase (RT)-PCR. An assay detecting antibodies to the envelop protein E2 (anti E2) of HGV has been developed and this serological marker is considered to be an indicator of the virus clearance [6,7]. Thus; the presence of anti E2 seems to indicate past HGV exposure and is associated with immunity and protection from reinfection [8]. Blood transfusion is the main risk factor for HGV transmission [9]. Patients with chronic renal failure (CRF) usually require frequent blood transfusions which make them more vulnerable to HGV infection [10,11]. The present data on the prevalence of HGV anti E2 in HD patients is conflicting, with studies showing rates of 7% in Japan [12] up to 29% in Germany [13]. Up to our knowledge there are no published data on the prevalence of HGV infection in Egyptian children with CRF. HGV associated hepatitis runs with normal biochemical parameters in 75% of patients [14]. Although HGV infection appears to.