CELLULAR IMMUNITY IN INFECTIOUS-MONONUCLEOSIS .2. SPECIFIC REACTIVITY TO EPSTEIN-BARR VIRUS-ANTIGENS AND CORRELATION WITH CLINICAL AND HEMATOLOGIC PARAMETERS

  • 1 January 1978
    • journal article
    • research article
    • Vol. 121  (4) , 1239-1244
Abstract
Infectious mononucleosis (IM) patients, Epstein-Barr virus (EBV)-seropositive and seronegative healthy donors and patients with other viral infections were tested for lymphocyte blastogenesis (LB) with phytohemagglutinin and 6 EBV (virus concentrate, culture supernatant and soluble [S] antigen) or control antigens. Fluorescent antibodies to EBV viral capsid antigen of Ig[immunoglobulin]G, IgM and IgA specificities, to nuclear antigen (EBNA) and heterophile antibodies were also assayed. These were correlated with clinical parameters (fever, pharyngitis, adenopathy, hepatitis, splenomegaly, atypical lymphocytes and total mononuclear cell counts). EBV viral and S antigen-induced LB was significantly greater in seropositive donors. IM patients had antigen-specific LB below that of seropositive donors initially and low responses for the acute phase of illness when clinical symptoms were present and antibody titers were maximal. Specific LB rose to a peak at 3.5-9 wk when the patients recovered, most laboratory findings returned to normal and antibodies declined. At peak, specific LB in IM patients exceeded that of seropositive donors, but later declined. Specific cell-mediated immunity (CMI) to EBV may develop slowly in IM in contrast with the evolution of the clinical events and humoral immunity. CMI probably is the mechanism of terminating lymphoproliferation in IM.