PREVALENCE OF HGV AND TTV INFECTION IN CHILDREN WITH CRYPTOGENIC CHRONIC HEPATITIS

Abstract

23 Recently, two new viruses: hepatitis G virus (HGV) and transfusion-transmitted virus (TTV) have been identified as aetiological agents of both post-transfusion and community acquired hepatitis. Aim of the present study was to evaluate the prevalence of HGV and TTV infection in children with cryptogenic chronic hepatitis (CCH). Methods: 46 children (24 males; mean age 6.9 years; range 1.5-17 years) with CCH was studied. CCH was diagnosed when serum alanine aminotransferase levels were more than 1.5 times normal levels for over 6 months without any apparent cause of liver disease. No patient had acute symptomatic onset or had received a blood transfusion. All appeared healthy during follow-up (median 4.2 years; range 1-10 years). HGV-RNA was detected by RT-nested PCR with primers from the NS-5 region of HGV. TTV-DNA was detected by semi-nested PCR with TTV-specific primers derived from two conserved regions of the published sequences. Results: Serum HGV-RNA was dected in 2 girls (4%) (aged 8 and 13 years), serum TTV-DNA was found only in a 6-year old boy (2%). One of the 2 HGV-infected girls and the TTV-infected patient showed mild hypertransaminasemia (about 1-1.5 folds the upper normal value) during the entire period of observation. The other HGV-infected girl showed fluctuating levels of ALT with peaks of 10-20 folds the upper normal value. Only in this patient liver biopsy was performed and evidence of steatosis, portal fibrosis and septa was found. After HGV-infection and TTV-infection were identified in these 3 children, their family members were screened for HGV and TTV infection, respectively. The mother of an HGV-infected girl and the father of the TTV-infected boy showed in serum HGV-RNA and TTV-DNA, respectively. The other HGV-infected girl had as only risk factor a minor surgical procedure in the clinical history. The parents who were found HGV- and TTV-infected, respectively, were healthy looking, had ALT in the normal range and did not report any over risk factor for viral hepatitis in their clinical history. No history of blood contacts between TTV-infected father and his TTV-infected child was reported; furthermore, it is to note that the mother did not show TTV-DNA in serum in two occasions. None of 5 siblings showed evidence of HGV or TTV infections. Conclusions: HGV and TTV seem to play a minor role in children with CCH. In 2 of 3 studied cases an intrafamilial transmission was observed. Although HGV and TTV infection in the majority of the cases are not associated with a significant liver damage, in our experience an HGV-infected girl showed evidence of severe hepatitis.