Lack of known hepatitis virus in hepatitis-associated aplastic anemia and outcome after bone marrow transplantation

Abstract

Summary:Viral infection has been shown to induce aplastic anemia, unidentified types of hepatitis being the most common cause for aplastic anemia-associated viral hepatitis. The survival rate for this group of patients after bone marrow transplantation with stem cells from an HLAmatched sibling is not well known. The aim of this study was to determine the prevalence of hepatitis G virus (HGV) and transfusion transmitted virus (TTV) infection in non-A, non-B, non-C hepatitis associated-aplastic anemia (HAAA) patients, and to define the role of bone marrow transplantation (BMT) as a therapeutic modality for this disease.

A study of bone marrow failure syndrome in children

“…[12,14] However, in the present study, only one (2%) patient had evidence of hepatitis B infection. We did not come across any other Indian studies to compare the results.…”

Analysis of T-cell repertoire in hepatitis-associated aplastic anemia

“…Although we cannot conclude whether the same or different antigens are involved in this broad stimulation, our data are suggestive of a similar pathogenic mechanism, perhaps triggered by an antigenspecific immune response as in viral hepatitis and supporting the hypothesis, based on epidemiologic and clinical investigations, that an unknown pathogen may be involve in this disease. 27 Some studies using peptides as antigens have suggested a limited T-cell response, with different clones having the same or related CDR3 sequences. 28,29 Shared CDR3 sequences have been harder to identify in hepatitis infections, although putative shared motifs have been suggested.…”

“…4 The presumed infectious cause of the hepatitis is unknown, but most cases are seronegative for known hepatitis viruses, including hepatitis A, B, C, and G (GB virus C[GBV-C]). [5][6][7] We previously reported 10 cases of HAA seen at the National Institutes of Health (NIH) that had evidence of lymphocyte activation; 70% responded to immunosuppression with antithymocyte globulin and cyclosporine. 8 Apart from case reports, the presence of lymphocyte activation, 9,10 and the clinical response to either immunosuppression or bone marrow transplantation, 11 little is known of the immunopathogenesis of this syndrome.…”

TT virus infection: a novel virus-host relationship

“…Therefore, it is possible that TTV may have a similar adverse effect on bone marrow function, particularly in association with immune suppression. Indeed, some reports link TTV replication to thrombocytopenia and aplastic anaemia [29][30][31]. Of great potential interest is the possibility that many of the haematological complications of AIDS, such as neutropenia, thrombocytopenia and anaemia may be the direct result of increased TTV replication in the bone marrow.…”