In order t o examine the role of Epstein-Barr virus (EBV) in the immortalization of human B lymphocytes and in the pathogenesis of lymphoid malignancies, we investigated whether the EBV integration into the human genome is randomly distributed or whether the virus integrates preferentially at certai
Re-exposure of human lymphoblastoid cell lines to Epstein-Barr virus
✍ Scribed by Volker Diehl; Hans Wolf; Heinrich Schulte-Holthausen; Harald Zur Hausen
- Publisher
- John Wiley and Sons
- Year
- 1972
- Tongue
- French
- Weight
- 760 KB
- Volume
- 10
- Category
- Article
- ISSN
- 0020-7136
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Human lymphoblastoid lines of various origins which harbour Epstein‐Barr virus (EBV)‐specific nucleic acid were re‐exposed to EBV. Following infection, cells of the non‐virus‐producing lines, Raji and S 95, predominantly synthesized EBV‐specific early antigens (EA), whereas only a small percentage of cells revealed viral capsid antigens (VCA). In Raji cells, the number of VCA‐producing cells was paralleled by the percentage of virus‐specific DNA‐synthesizing cells. In S 95 cells, however, viral DNA‐synthesizing cells exceeded the number of VCA‐producing cells by a factor of more than 10. Induction of EA in Raji cells was dose‐dependent and inversely related to cell growth. Irradiation of the virus by ultraviolet light prior to infection led to reduced infectivity. This reduction seemed to follow single‐hit kinetics. Raji cells, previously re‐exposed to EBV, showed reduced EA induction after re‐infection with EBV, as compared to Raji control cells not previously exposed. Of 10 lines which spontaneously synthesize EBV‐specific antigens, seven lines proved to be refractory to re‐infection, whereas three were as susceptible as the Raji and S 95 controls. From three of the refractory lines infectious virus could be recovered from the culture medium prior to infection.
These results permit the following interpretations: (1) the response of human lymphoblastoid cells after re‐infection with EBV results from the infecting virus and not from stimulation of endogenous genomes; (2) cells demonstrating EA synthesis ultimately die; (3) re‐exposure to EBV increases the resistance to re‐infection of the surviving cells; and (4) cell lines producing infectious EBV are refractory to re‐infection. It is suggested that the spontaneous synthesis of infectious virus favours the selection of resistant cells.
📜 SIMILAR VOLUMES
## Abstract Redistribution and consequent cap formation of Epstein‐Barr virus adsorbed to human lymphoblastoid cells were studied by indirect membrane immunofluorescence carried out at 0° C. When EBV was adsorbed on cells at 0° C, the cell sur face fluorescence had a mostly ring‐like pattern. Howev
## Abstract Twenty‐nine lymphoblastoid lines and one IgE‐producing myeloma line of human origin were exposed to Epstein‐Barr virus (EBV) concentrates __in vitro__. The adsorption of the virus to the outer cell membrane was assessed by counting the number of direct membrane fluorescence‐positive cel
## Abstract The tumor promoter TPA (12‐0‐tetradecanoyl‐phorbol‐13‐acetate) efficiently induces the synthesis of Epstein‐Barr virus (EBV) antigens in EBV‐genome‐harboring human lymphoblastoid cells. We attempted to obtain information on the binding of TPA to cells and on the relationship between TPA
## Abstract Differential induction of Epstein‐Barr virus (EBV)‐related antigens was observed after Sendai virusmediated fusion of producer and non‐producer cells with various human and mouse cells. The EBV‐determined early nuclear antigen (ENA), early antigen (EA) and viral capsid antigen (VCA) cou