## Abstract Two human lymphoblastoid cell lines were established by the transformation of human cord‐blood lymphocytes with transforming Epstein‐Barr virus (EBV). One cell line (HLB‐R1) was established with EBV obtained after the superinfection of Raji cells with HR‐1 EBV and the other (HLB‐B1) was
Sensitivity of Epstein-Barr virus (EBV) producer and non-producer human lymphoblastoid cell lines to superinfection with EB-virus
✍ Scribed by George Klein; Laszlo Dombos; Balwant Gothoskar
- Publisher
- John Wiley and Sons
- Year
- 1972
- Tongue
- French
- Weight
- 928 KB
- Volume
- 10
- Category
- Article
- ISSN
- 0020-7136
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✦ Synopsis
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 cells immediately after infection and by the direct radioimmune membrane labelling method. Reference reagents were derived for both tests from the same serum (“Agnes”), containing antibodies against EB‐viral envelope and capsid antigens. The intracellular course of infection was followed by counting the number of cells that responded with the development of early antigen (EA) 48 h after infection. The 11 lymphoblastoid lines that produced no EBV‐determined membrane and early antigens adsorbed the virus, although there were quantitative differences between them. EA‐positive cells appeared in significant numbers in only seven of them, however. Four lines remained EA negative in spite of a relatively good adsorbing capacity. The IgE‐producing myeloma line showed neither virus adsorption nor EA development.
Eighteen lymphoblastoid lines were “producers”, or “abortive producers”, __i.e.__a small proportion of the cells continuously generated two or three of the immunofluorescence‐detectable viral antigens, MA, EA and VCA. Nine lines failed to adsorb significant virus quantities and showed no certain increase of EA‐positive cells. The resistance of these lines to superinfection is probably determined at the level of viral receptors. Five lines showed a relatively good virus adsorption, but this was not followed by any significant increase in the number of EA‐positive cells. Four lines showed good adsorption and also responded with a significant increase in the number of EA‐positive cells.
The same responses can thus be found to EBV‐superinfection in producer and non‐producer lines, but the producer lines show a strong preponderance of superinfection‐resistant lines with an adsorption block at the receptor level.
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