Prevalence and clinical features of hepatitis G virus infection in bone marrow allograft recipients

Abstract

Summary:Although HGV infection appears clinically benign in the vast majority of cases and although no causal relationship between HGV and hepatitis has been established, 6,7 some To study the prevalence and clinical features of hepatitis G virus (HGV)/GB virus C (GBV-C) infection in bone authors 8 have suggested that HGV is responsible for fulminant hepatitis and aplastic anemia. 9,10 Furthermore, marrow transplantation (BMT), we examined frozen serum samples from 95 bone marrow allograft patients reports of chronic HGV carriers and of the high prevalence of HGV-positive blood donor populations 5,11,12 raise the for HGV/GBV-C RNA by RT-PCR. Twenty-eight out of 95 (29.5%) were positive and 14 of the HGV ϩ patients problem of a high risk of infection in multiply transfused and immunosuppressed patients. were already positive before transplantation. The mean numbers of blood donors to whom the HGV − and HGV + For these reasons, we have retrospectively studied the incidence and clinical features of HGV infection in 95 bone populations were exposed before BMT were not significantly different (Kruskal-Wallis test, P = 0.08, NS) but marrow allograft patients. did reveal that the HGV + population had been transfused more often. Moreover, all but one of the patients who were HGV + before graft, had had hematological diseases which needed heavy transfusion protocols sugMaterial and methods gesting, a role of blood products in HGV transmission. Fifty out of the 95 patients received Gammagard intravenous immunoglobulin (IVIG) batches suspected ofPatients having transmitted HCV. However, no significant difference appeared between these recipients and those Ninety-five patients allografted in Saint-Louis Hospital (Paris), between 1985 and February 1996 with a follow-up receiving other IVIG. Despite their immunodeficiency, no clinical or biological evidence of liver disease potenof at least 6 months were studied. Eighty-three (87.4%) were grafted with family HLA-identical donors, 11 (11.6%) tially linked to HGV infection has as yet been observed. The clinical outcome, in terms of acute GVHD, chronic with unrelated HLA matched donors and one with cord blood (1%). The median survival was 3 years and 3 months GVHD or veno-occlusive disease was similar in HGV + and HGV − recipients suggesting the absence of adverse (range 7 months-11 years). There were 60 males and 35 females with a mean age of 26 years (range 2-59). Among effects of HGV infection on the early outcome of allogenic BMT. Long-term evolution remains to be prospecthese patients, 29.5% (28/95) had chronic myeloid leukemia, 34.7% (33/95) acute leukemia, 9.4% (9/95) Fanconi tively studied. Keywords: BMT; hepatitis G virus; GBV-C; GVHD; disease, 7.4% (7/95) non-Hodgkin lymphoma, 11.5% (11/95) severe aplastic anemia, 5.4% (5/95) myelodyspla-VOD sia, 1.05% (1/95) chronic lymphoid leukemia and 1.05% (1/95) paroxysmal nocturnal hemoglobinuria. After transplantation, recipients were followed-up at 3, Despite the discovery of HCV, 1 about 12% of post-trans-6 and 12 months or...

Long-term liver function of recipients with hepatitis G virus infection after bone marrow transplantation

“…The presence of HGV infection or HCV infection before BMT was not a predictor of VOD in our studies, which was consistent with the results of other reports. 12,13,18 There has not been a report on the long-term follow-up of bone marrow recipients with HGV infection. None of the patients became HGV-RNA negative within 5 years in our study.…”

“…These results were consistent with those of other reports. [11][12][13]15 Two patients in the GϩCϩ group developed fulminant hepatitis and died on days 139 and 148. 10 We think it would be reasonable, from comparison between the GϩCϩ group and the GϩCϪ group, to say that the fulminant hepatitis in these two patients should be ascribed to HCV infection and not HGV infection, although there is a report which suggests that HGV can be responsible for fulminant hepatitis.…”

Autoimmune diseases and autoimmunity post-bone marrow transplantation

“…These observations carry important clinical applications: since it has been demonstrated that monoclonal antibodies can eliminate CD13positive cells, and consequently completely inhibit CMV replication, 75 elimination of these cells in BM grafts pretransplant can decrease the risk of CMV complications, including chronic GVHD. 75 Nevertheless, it should be noted that although CMV could contribute to emergence of autoimmunity in the post-BMT setting via molecular mimicry (as opposed to hepatitis G virus, 76 for example), the fact that not all recipients who have CMV infection develop chronic GVHD or an autoimmune disease, further demonstrates that autoimmune diseases are multifactorial in etiology. CMV per se is not sufficient alone, and another contributory factor towards autoimmune problems, such as genetic predisposition, is required.…”

Characterization of human pegivirus infection in liver transplantation recipients

“…Similarly, Kallinowski et al also showed that heart‐transplanted patients had higher prevalence (HPgV positive; 18/50, 36%), there were no significant difference in clinical outcomes, such as rejection. Moreover, Corbi et al described that bone‐marrow allograft recipients had higher prevalence (HPgV positive; 28/95, 29.5%), there were no significant difference in acute or chronic graft vs host disease. As described above, patients who received other types of organ transplantation besides LT also had higher prevalence of HPgV infection.…”