Pure red blood cell aplasia associated with chronic Epstein-Barr virus infection: evidence for T cell-mediated suppression of erythroid colony forming units.

A prominent T cell suppressor response is known to develop and inhibit the polyclonal B cell activation induced by Epstein-Barr virus infection. Exuberant T suppressor cell activity suppressing erythropoiesis has been demonstrated in certain cases of pure red blood cell aplasia. We studied a 19-year-old man who developed pure red cell aplasia after Epstein-Barr virus infection. Over a 70-week period, lymphocyte function and serologic evidence for chronic Epstein-Barr virus infection was demonstrated. On two separate occasions, no evidence for serum inhibition of bone marrow erythroid colony formation in methylcellulose was observed. Growth of granulocyte-macrophage progenitors from the patient's bone marrow was normal. The patient's bone marrow cultures yielded 81.6 +/- 11.2 erythroid colony-forming units per 10(5) bone marrow mononuclear cells, which was approximately 50% of levels in normal control bone marrow. Culture of peripheral blood mononuclear cells for erythroid burst-forming units revealed minimal growth (less than 1% of control values). Depletion of bone marrow T cells by E-rosetting resulted in a threefold increase in erythroid colony-forming units in the patient's bone marrow but no significant increase from control bone marrow. In the patient, addition of bone marrow T cells but not peripheral blood T cells significantly suppressed autologous erythroid colony-forming unit proliferation from T cell-depleted bone marrow. These results suggest that the pure red cell aplasia associated with chronic Epstein-Barr virus infection in this case was caused by bone marrow T cell-mediated suppression of erythroid colony-forming unit proliferation.