PATHOGENESIS AND TREATMENT OF APLASTIC ANEMIA

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Aplastic anemia and other forms of bone marrow failure have clinical and laboratory features consistent with a possible viral etiology followed by immunological pathophysiology. Aplastic anemia may follow on a viral infection, especially non-A non-B hepatitis or infectious mononucleosis. Patients have evidence of activation of their immune system similar to that observed in many viral infections, including activation of cytotoxic lymphocytes, excessive lymphokine production, and decreased natural killer cell activity and number. We have previously reported the presence of Epstein-Barr virus in the bone marrow of some patients with aplastic anemia. With the recent cloning of the etiologic agent for non-A non-B hepatitis, termed hepatitis C, we have searched for such viral sequences in the bone marrow and blood of these patients. We have sought evidence of virus infection using a commercial assay for antibody to a nonstructural protein of hepatitis C, and in our own laboratory we have developed a sensitive and accurate polymerase chain reaction method for detection of hepatitis C sequences. Based on our previous work with dengue, also a flavivirus, in which viral propagation was demonstrated in hematopoietic cells, we have attempted to inoculate hepatitis C into hematopoietic cell lines and explanted bone marrow cultures. Hepatitis C is present in the bone marrow and blood of a subset of patients with aplastic anemia, but in most cases the presence of the virus is correlated with the development of transfusion-associated hepatitis and not present at outset.