• 1 January 1981
    • journal article
    • research article
    • Vol. 41  (11) , 4222-4225
Abstract
Since B-lymphocytes are targets and a continuing habitat of Epstein-Barr virus (EBV) and the cell-mediated immune system becomes secondarily involved, primary and persistent EBV infections in immunologically compromised individuals can take unusual courses. Depending on the immunological defect, the clinical, hematological and serological responses to primary EBV infections may be more or less pronounced than in immunologically competent patients. Infectious mononucleosis has per se an immunosuppressive effect which may enhance a preexisting immune defect. The persisent latent viral carrier state which regularly ensues after the primary EBV infection may become decontrolled by immunosuppressive diseases or therapy, leading rarely to illnesses referable to the virus but often to increases in the titers of antibodies to viral capsid and early antigens and/or declines in the antibody titer to EBV-associated nuclear antigen. Absence or dysfunction of different leukocyte subpopulations may account for the differential changes in antibody patterns.