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J Gen Virol 48 (1980), 111-121; DOI 10.1099/0022-1317-48-1-111
© 1980 Society for General Microbiology

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Isolation of a Virus Closely Related to Gibbon Ape Leukaemia Virus from Cells Infected with Virus (HL-23V) Released by Human Leukaemic Cells

Carolyn M. Bergholz1, Lauren G. Wolfe2, Gregory A. Schulz2, Friedrich Deinhardt3, Nancy R. Miller4 and Marvin S. Reitz5

1 Department of Microbiology and Schools of Basic Medical Sciences and Clinical Medicine, University of Illinois, Urbana, Illinois 61801, U.S.A.
2 Department of Microbiology, Rush-Presbyterian-St Luke's Medical Center, Chicago, Illinois 60612, U.S.A.
3 Max von Pettenkofer-Institute, Munich, West Germany
4 Bethesda Research Laboratories, Rockville, Maryland 20850, U.S.A.
5 Laboratory of Tumor Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014, U.S.A.

Canine thymus cells infected with virus (HL-23V) produced by human acute myelogenous leukaemia cells in culture were shown in previous reports to produce transforming and non-transforming type C virus similar or identical to the simian sarcoma virus complex SSV(SSAV) and to induce tumours in marmoset monkeys (Bergholz et al. 1977a). In these earlier studies the appearance of breakthrough foci at low dilutions of antiserum in neutralization tests with high-titred anti-SSV(SSAV) serum suggested the presence of another virus, distinct from SSV-(SSAV). We now report the isolation of this component and, by comparative neutralization analysis, demonstrate that it is most closely related to gibbon ape leukaemia virus (GALV). It is distinguished from SSV(SSAV) by kinetics of neutralization and molecular hybridization experiments. This component was readily cloned both from virus produced by HL-23V chronically-infected canine thymus cells established by Teich et al. (1975) when HL-23V was first isolated and from virus produced by HL-23V-induced marmoset tumour cells in culture. The presence of this component in the original leukaemic cell cultures is discussed.

Received 26 June 1979; accepted 17 December 1979.





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