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The action of dna antagonists on epstein‐barr virus (EBV)‐associated early antigen (EA) in burkitt lymphoma lines
Author(s) -
Gergely Lajos,
Klein George,
Ernberg Ingemar
Publication year - 1971
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910070214
Subject(s) - antigen , raji cell , cell culture , microbiology and biotechnology , dna synthesis , burkitt's lymphoma , virus , virology , capsid , dna , biology , lymphoma , epstein–barr virus , thymidine , immunofluorescence , antibody , immunology , biochemistry , genetics
Abstract The effect of two DNA antagonists (IUDR and Ara C) on EBV‐associated antigens was studied in two BL‐derived carrier culture lines (P3HR‐1 and Onesmas). Both drugs led to an accumulation of the early antigen (EA) from 2% in the untreated to 5–40% in the treated cultures. Ara C blocked the production of viral capsid antigen (VCA) whereas a small number of VCA + cells were still present after IUDR treatment. Reversion of Ara C‐induced DNA inhibition led to the appearance of VCA + cells, reaching a higher level than in the untreated control samples. Combined immunofluorescence and autoradiography showed that the majority of VCA + cells incorporated H 3 ‐thymidine. These facts are in line with the hypothesis that EA can be made in the absence of cellular DNA synthesis, whereas VCA production is dependent on the DNA synthesis. The relationship between EA and two other EBV‐associated antigens, MA (membrane antigen) and VCA (viral capsid antigen) was studied by the two‐color immuno‐fluorescence technique. VCA + cells were EA+ and MA+. EA + VCA ‐ cells were partly MA + and partly MA‐. This is in good agreement with the corresponding findings on the EBV‐infected Raji cell system (Gergely et al. , 1970a).