Delayed Onset of Infectious Mononucleosis Associated with Acquired Agammaglobulinemia and Red Cell Aplasia

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Abstract
In 1974, an 11 yr old white boy with the X-linked lymphoproliferative syndrome developed hyper-IgM after becoming infected with Epstein-Barr virus. He failed to develop normal immune responses against the virus. In Dec. 1981, when red cell aplasia occurred, he was given packed erythrocytes and .gamma.-globulin. Nine wk later, acute infectious mononucleosis developed. Concurrently, his T4/T8 helper/suppressor ratio decreased from 2.7 to 0.2 and IgM antibodies to Epstein-Barr virus appeared. Subsequently, circulating B cells became undetectable in his blood, and agammaglobulinemia appeared. Red cell aplasia abated transiently. This patient''s course was complicated by Haemophilus influenzae and Mycobacterium tuberculosis pneumonias, and red cell aplasia and agammaglobulinemia persisted. Epstein-Barr virus acting as a slow virus probably induced the red cell aplasia and agammaglobulinemia because of the aberrant immune responses to Epstein-Barr virus. Immunodeficient responses to Epstein-Barr virus should be sought in other patients with the disease documented in this patient.