Angioimmunoblastic lymphadenopathy after infectious mononucleosis.

Angioimmunoblastic lymphadenopathy occurred in a 46-year-old man 16 months after an episode of infectious mononucleosis induced by Epstein-Barr (EB) virus. The features of infectious mononucleosis included fever, pharyngitis, lymph gland enlargement, hepatosplenomegaly, hyperbasophilic mononuclear cells, and IgM antibodies to EB virus, although heterophile antibodies were not detected. The illness was severe and prolonged and included an asymptomatic measles virus infection. Over a year later massive enlargement of the lymph nodes led to a biopsy, which showed a diffuse infiltration with lymphoid cells and a proliferation of arborising small vessels typical of angioimmunoblastic lymphadenopathy. In spite of corticosteroids, levamisole, chlorambucil, and radiotherapy, no remission occurred, and serious infections led to death 18 months after the onset. Viral infections with EB virus and measles virus associated with pre-existing or subsequent immunological changes probably resulted in the appearance of angioimmunoblastic lymphadenopathy.     

Cytotoxic lymphocytes in infectious mononucleosis.

Seven patients with a clinical diagnosis of infectious mononucleosis (IM) and detectable heterophil antibodies were found to have peripheral blood lymphocytes that were cytotoxic for lymphoid cells containing Epstein-Barr virus from a patient with Burkitt''s lymphoma. The cytotoxic lymphocytes persisted in the peripheral circulation for up to 45 days. Patients who had had IM 1 to 5 years previously lacked such cytotoxic lymphocytes. Patients who had signs and symptoms of IM but no detectable heterophil antibodies lacked cytotoxic lymphocytes. The lymphocytes of one patient with IM showed progressive diminution of cytotoxic ability after prednisone treatment.     

Lymphocyte subpopulations and reactivity during and after infectious mononucleosis

T- and B-lymphocyte numbers, as well as lymphocyte reactivity to mitogens in vitro, were studied and correlated to other laboratory tests during the acute phase of infectious mononucleosis (30 patients) and up to one year thereafter. During the acute disease an absolute increase in both T- and B-lymphocyte numbers was recorded, the relative increase in B-lymphocytes occurring at the start. B-lymphocyte numbers fell after the second week and T-lymphocyte numbers after the fourth week of disease. Lymphocyte activation was impaired in all patients during the acute phase and was still significantly impaired for some mitogens after 6-9 months. Very few correlates between lymphocyte tests and other laboratory and clinical parameters were found.