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.     

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.     

Viral antibodies in infectious mononucleosis

Abstract Patients with Epstein-Barr virus (EBV) infectious mononucleosis (IM) usually develop heterophilic antibodies and some autoantibodies. Antibodies to rubella, measles, adeno-, entero-, herpes simplex, cytomegalo- and varicella-zoster viruses were titrated in sera from IM patients and matched healthy controls using the complement fixation test (CFT) and the haemagglutination inhibition test. Except for herpes simplex virus and cytomegalovirus, the IM sera had significantly higher arithmetical and geometrical mean antibody titres and showed in most cases higher antibody prevalences in the CFT. The titre rise was most pronounced for rubella and measles antibodies, between 2- and 3-fold. There were no cases of very high titres occasionally seen in IM. The IM sera had higher total IgG serum levels than the controls, 17.27 g/1 and 11.8 g/1, respectively ( P < 0.001). The present data show that in addition to previously reported high levels of some autoantibodies and of heterophilic antibodies, there is a more general increase in IgG antibodies to commonly occurring viruses. This increase is most likely due to the polyclonal activation of B-lymphocytes following the binding of EBV to the complement receptor CR2 (CD21). When due consideration is given to the possible occasional occurrence of a false positive rubella IgM test, the raised antibody-titres will most likely not interfere with routine diagnostics.