Antibodies to eb virus capsid antigen and to soluble antigen of lymphoblastoid cells in infectious mononucleosis patients

Abstract

Sera from inlfectious mononucleosis patients aged 2 to 35 years and from normal subjects aged I I to 35 years were examinedfor the presence of antibody to the EB virus capsid antigen ( V C A ) Extracts of Burkitt lymphoma and other lymphoblastoid cell lines contain a soluble (S)antigen demonstrated by complement-fixation (CF) test (Armstrong P I ul., 1966;Vonka et al., 1969;1970a; 1970b;Pope et al., 1969;Gerber and Diehl, 1970). This antigen was found in both EB-virus-positive and -negative cell lines and was immunologically distinct from the viral capsid antigen (VCA) as detected by immunofluorescence (IF) or CF test. The S antibody, although present in many human sera, was never found in sera which were free of antibody to VCA. This indicates that EB virus infection is the pre-requisite for the S antibody development. On the basis of these observations the suggestion was made that the S antigen is an EB virus coded non-structural antigen.When studying the age distribution of VCA and S antibodies in human sera we found that 50 to 70% of subjects over 1 year of age, whose sera were VCA-positive, also possessed the S antibody. The antibody pattern was markedly different in children aged 6 to 12 months: only one out of 15 VCA-positive subjects in one group (Vonka et al., 1970a) and none of 30 VCApositive in the other group (Vonka and BenyeshMelnick, 1970) possessed the S antibody. The absence of S antibody in VCA-positive subjects aged 6 to 12 months, i.e. subjects most probably infected with EB virus only recently,

Nasopharyngeal carcinoma. IV. Evolution of complement‐fixing antibodies during the course of the disease

“…Patients with infectious mononucleosis, where primary EBV infection is accepted as the cause of the disease, usually do not have detectable C F antibodies against S antigen during the acute clinical phase and develop such antibodies later (3 months to 1 year) after the clinical syndrome has disappeared (Sohier, 1971;Vonka et a[., 1972). In contrast, the high C F reactivity to S antigen of NPC patients at stage I, comparable to that of NPC patients at stage IV of the disease, favours a long-standing and important infection before the clinical expression of NPC, and should eliminate the hypothesis of a primary EBV infection as the immediate cause of the tumour.…”

The Herpesviruses

“…Many compounds have been shown to induce EB viral expression in latently infected cells: halogenated pyrimidines [5-iodo-2-deoxyuridine (IUdR) or 5-bromodeoxyuridine (BUDR)] Glaser et al, 1976); tumor promoters, such as the phorbol ester 12-0-tetradecanoyl phorbol-13 acetate (TPA) , antibodies to surface immunoglobulin M (lgM) (Tovey et al, 1978); heat (Vonka and Kutinova, 1973); and even platinum compounds (Vonka et al, 1972). TPA represents the most active compound of croton oil, extracted from seeds of Euphorbia.…”

“…An inhibitor of DNA synthesis, n-butyrate, is also an inducer of EA expression (Luka et al, 1979;Saemundsen et al, 1980). Some lines are induced to produce veA by heat, UV irradiation, and even platinum compounds (Lai et al, 1973;Vonka and Kutinova, 1973;Vonka et al, 1972). In no instance is there clear understanding of the mechanisms behind induction.…”

Effects of n-Butyrate and phorbol ester (TPA) on induction of Epstein-Barr virus antigens and cell differentiation

“…The T P A was included in the s t u d y as it has frequently been claimed to interfere with cellular differentiation (3,9,12,20,21,29,31). The effects of these drugs were also followed in another virus non-producer cell line NC37.…”