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Incidence and Influence of GB Virus C and Hepatitis C Virus Infection In

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Incidence and Influence of GB Virus C and Hepatitis C Virus Infection In Bone Marrow Transplantation, (1998) 21, 1131–1135 1998 Stockton Press All rights reserved 0268–3369/98 $12.00 http://www.stockton-press.co.uk/bmt Incidence and influence of GB virus C and hepatitis C virus infection in patients undergoing bone marrow transplantation H Akiyama1, N Nakamura1, S Tanikawa1, H Sakamaki1, Y Onozawa1, T Shibayama2, S Tanaka2, F Tsuda3, H Okamoto4, Y Miyakawa5 and M Mayumi4 1Hematology Division and 2Liver Unit, Tokyo Metropolitan Komagome Hospital, Tokyo; 3Department of Medical Sciences, Toshiba General Hospital, Tokyo; 4Immunology Division, Jichi Medical School, Tochigi-Ken; and 5Miyakawa Memorial Research Foundation, Tokyo, Japan Summary: bone marrow donors. Since most patients have underlying diseases impairing their immune system and receive mye- Markers of GB virus C (GBV-C) and hepatitis C virus loablative therapies before BMT, infection with hepatitis (HCV) were sought in 80 patients before and after they viruses tends to persist and may induce severe hepatitis. underwent BMT in a metropolitan hospital in Tokyo Furthermore, the infection may be modulated by the adop- between 1990 and 1996. RNA of GBV-C was detected tive immunity transferred by a bone marrow donor who has in 14 (18%) patients before BMT. Of the 55 patients been infected or who has overcome the infection. who had been transfused, 14 (25%) possessed GBV-C Recently, a putative hepatitis virus designated GB virus RNA at a frequency significantly higher than in the 25 C (GBV-C) or hepatitis G virus (HGV) has been disco- untransfused patients who were all negative (P Ͻ 0.01). vered.2,3 For the sake of convenience these are collectively HCV RNA was detected in three of the 55 (5%) trans- referred to here as GBV-C. This is a positive, single- fused patients, but in none of the 25 untransfused stranded RNA virus of approximately 9400 bases and patients. Sera at 3 months after BMT were available for classified in the Flaviviridae family. GBV-C prevails 57 patients. GBV-C RNA persisted in all 10 patients worldwide, as estimated by the detection of its RNA in 1– who were infected before BMT, while it was detected in 5% of apparently healthy blood donors.3–7 GBV-C is trans- five of the remaining 47 (11%) patients who were not. mited by transfusion and intravenous drug abuse.5,8–11 Co- However, persistent and/or ongoing GBV-C infection infection with GBV-C and HBV or HCV is frequent in had no appreciable influence on patient morbidity or patients with chronic liver disease and in intravenous drug mortality. Two of the 57 patients were positive for HCV users.3,8 GBV-C infection persists in patients with compro- RNA before BMT and this persisted after BMT in both. mised immunity, such as those on maintenance hemodia- HCV RNA became positive in eight of the remaining 55 lysis.5 The ability of GBV-C to induce hepatitis has, how- (15%) patients who were negative before BMT. Of the ever, as yet, not been established. 14 patients who received transfusions screened by the Evidence of infection with GBV-C, HCV and HBV was first-generation test at BMT, seven (50%) became posi- sought in patients with malignant hematological diseases or tive for HCV RNA, a rate significantly higher than the aplastic anemia before and after they underwent BMT, and one of 41 (2%) patients who received transfusions the results were correlated with the number of transfusions screened by the second-generation test (P Ͻ 0.001). they received before and at the time of transplantation. These results indicate that BMT patients are at increased risk of GBV-C infection transmitted by trans- fusions received before and at the time of BMT, and Patients and methods that the risk of HCV infection has decreased after the implementation of the second-generation anti-HCV test. Study population Keywords: GBV-C; HCV; BMT From July 1990 to August 1996, a total of 155 patients underwent BMT in the Hematology Division of Tokyo Metropolitan Komagome Hospital. Only the patients who Patients undergoing BMT are at increased risk of infection underwent allogeneic BMT and whose pre-BMT sera are with blood-borne hepatitis viruses such as hepatitis B virus available were included in this retrospective study. One (HBV) and hepatitis C virus (HCV), which poses serious hundred and twenty-four patients received allogeneic or 1 problems. These viruses are mainly introduced either by syngeneic BMT and in 80 patients, pre-BMT sera were the transfusions they received before and at BMT or by the available (Table 1). They included 44 males and 36 females with the mean (Ϯs.d.) age of 32 (Ϯ9) years. During BMT, complete blood counts were performed Correspondence: Dr H Akiyama, Hematology Division, Tokyo Metropoli- tan Komagome Hospital, 3–18–22, Honkomagome, Bunkyo-ku, Tokyo, three times a week and blood chemistries obtained two to 113, Japan three times a week. Patients were evaluated retrospectively Received 12 September 1997; accepted 29 December 1997 for veno-occlusive disease (VOD) by the criteria of GBV-C and BMT H Akiyama et al 1132 Table 1 Patient characteristics samples of 10-fold dilution of extracted RNAs were pre- pared, and the sample of the highest dilution positive for Characteristics GBV-C RNA was determined. The result was converted to represent the titer (10N) of the virus per ml of the test Age average (range) 32 (17–53) years serum. Sex M/F 44/36 Diagnosis CML 34 Markers of HCV and HBV infections AML 13 ALL 15 Until January 1992, blood transfused to patients was SAA 8 screened for antibody to HCV (anti-HCV) by the first-gen- MDS 8 Lymphoma 2 eration enzyme-linked immunosorbent assay (ELISA) Donor using Ortho ELISA I (Ortho Diagnostic Systems, Tokyo, related 67 Japan) and thereafter by the second-generation ELISA unrelated 11 (Ortho ELISA II; Ortho Diagnostic Systems). syngeneic 2 Sera from patients were serially diluted two-fold, and Preparative regimen BU/CY 53 anti-HCV was assayed by hemagglutination using Abbott Ara-C/CY/TBI 19 HCV PHA 2nd Generation (Dainabot, Tokyo, Japan). Sera CY/TLI 8 inducing hemagglutination at dilutions Ͼ25 were con- GVHD prophylaxis sidered to be positive for anti-HCV. RNA of HCV was CsA/MTX 76 ␮ Others 4 determined in RNAs extracted from 100 l of the test serum by a commercial kit (Amplicor HCV detection kit; SAA = severe aplastic anemia; MDS = myelodysplastic syndrome; TLI = Japan Roche, Tokyo, Japan). total lymphoid irradiation. Hepatitis B surface antigen (HBsAg) and the correspond- ing antibody (anti-HBs) were determined by serial two-fold dilutions of the test serum using commercial kits (MyCell; McDonald et al,12 GVHD, graft rejection, interstitial pneu- Institute of Immunology Co. Ltd, Tokyo, Japan), and hem- monia, hemorrhagic cystitis and varicella zoster virus infec- agglutination at dilutions у22 was considered reactive. tion. In 57, sera 3 months after BMT were also available, while in 23 patients, follow-up sera were not available even Statistical analysis though all survived for more than 3 months after BMT. Frequencies between groups were compared with the ␹2 test or Fisher’s exact test using StatView (Abacus Concepts, Bone marrow transplantation Berkeley, CA, USA). Group means were compared using Preparative therapy was given mainly according to the pri- the Student’s t-test. mary diseases and source of bone marrow. Patients with AML and CML were treated with busulfan 16 mg/kg and cyclophosphamide 120 mg/kg (BU/CY). Total lymphoid Results irradiation (TLI) was added in patients who received mar- row from unrelated donors. Patients with severe aplastic GBV-C, HCV and HBV markers before BMT anemia were treated with cyclophosphamide 200 mg/kg Table 2 gives prevalence rates of viral markers in the 80 and TLI 700 cGy (CY/TLI) and those with ALL were patients before BMT. GBV-C RNA was detected in 14 treated with Ara-C 8 g/m2 and cyclophosphamide 120 mg/kg, followed by total body irradiation (TBI), 1200 cGy (18%) patients, HCV RNA in three (4%) and HBsAg in none (P Ͻ 0.001). No patients were vaccinated against (Ara-C/CY/TBI). Other diseases were treated with BU/CY HBV. All three patients with HCV RNA were positive for or Ara-C/CY/TBI. All patients except for those undergoing syngeneic BMT received cyclosporine and short-term methotrexate as prophylaxis for GVHD. Table 2 Markers of GB virus C, hepatitis C virus and hepatitis B virus infections in patients before BMT Determination of GBV-C RNA Viral markers Total Transfusion P valuea n = 80 (%) ␮ RNAs were extracted from 100 l of serum with an extrac- (+)(−) tion reagent containing guanidinium isothiocyanate and n = 55 (%) n = 25 (%) phenol (ISOGEN-LS; Nippon Gene Co. Ltd, Tokyo, Japan) and dissolved in 5.3 ␮l of distilled water treated with GBV-C RNA 14 (18) 14 (25) 0 Ͻ0.01 diethylpyrocarbonate (Sigma Chemical, St Louis, MO, HCV RNA 3 (4) 3 (5) 0 USA). Samples were reverse transcribed and the cDNA was Anti-HCV 5 (6) 5 (9) 0 HBsAg 0 0 0 amplified by PCR using primers taken from well-conserved Anti-HBs 6 (8) 5 (9) 1 (4) areas in the 5′ untranslated region of the genome, by the 9 method described previously. aCompared between the patients with previous transfusions and those with- For semi-quantitative analysis of GBV-C RNA, serial out. GBV-C and BMT H Akiyama et al 1133 anti-HCV; no patients had seronegative HCV infection. GBV-C RNA in patients after BMT Previously transfused patients had a higher frequency of In 57 of 80 patients, sera obtained at 3 months after BMT GBV-C RNA than untransfused patients (14 of 55 or 25% were also available.
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