The action of dna antagonists on epstein‐barr virus (EBV)‐associated early antigen (EA) in burkitt lymphoma lines

The action of dna antagonists on epstein‐barr virus (EBV)‐associated early antigen (EA) in... 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 H3‐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). http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png International Journal of Cancer Wiley

The action of dna antagonists on epstein‐barr virus (EBV)‐associated early antigen (EA) in burkitt lymphoma lines

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Publisher
Wiley
Copyright
Copyright © 1971 Wiley‐Liss, Inc., A Wiley Company
ISSN
0020-7136
eISSN
1097-0215
DOI
10.1002/ijc.2910070214
Publisher site
See Article on Publisher Site

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 H3‐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).

Journal

International Journal of CancerWiley

Published: Mar 15, 1971

References

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