Antigens of Leukemias Induced by Naturally Occurring Murine Leukemia Virus: Their Relation to the Antigens of Gross Virus and Other Murine Leukemia Viruses

Antigenic determinants of p30, the most abundant internal virion protein of C type RNA viruses, were detected on the surface of spleen cells from mice bearing Moloney leukaemia and on an in vitro line of Moloney sarcoma, MSC. On both cell types, these determinants on the p30 molecules served as cytotoxic targets in a xenogenic complement dependent antibody mediated 51Cr release assay. Two antisera were used: a rat anti MLV -M induced lymphoma serum, and an antiserum raised in goats to either disrupted FeLV. The cytotoxic target antigens of these antisera were analysed by inhibition of cytotoxicity with viral and cellular proteins.

mentioning

confidence: 99%

Studies on mouse Moloney virus induced tumours: I. The detection of p30 as a cytotoxic target on murine Moloney leukaemic spleen cells, and on an in vitro Moloney sarcoma line by antibody mediated cytotoxicity

Epstein¹,

Knight²

1975

“…'An antigen common to murine C-type RNA tumour viruses has been demonstrated by various serological techniques, including immunodiffusion (Geering, Old and Boyse, 1966) complement fixation (Hartley et al, 1965) and immunofluorescence (Lejneva and Abelev, 1970) and has been shown to be an internal component of the virus particle (Schafer et al, 1969). For the detection of this antigen, termed the species or group specific (gs) antigen (Gilden and Oroszlan, 1971), sera were raised in heterologous hosts bearing neoplasms induced by the murine agents or by immunization with disrupted virus particles.…”

Section: Discussionmentioning

confidence: 99%

Antigens of Tumours Induced by Naturally Occurring Murine Sarcoma Virus (MSV-FBJ)

Jones¹,

Moore²

1974

Summary.-Antigens associated with cells transformed in vivo by FBJ virus, a wild type murine sarcoma virus (MSV) complex originating from a spontaneously arising osteosarcoma in a CF1 mouse, have been partially characterized by complement fixation (CF). Using rat antisera against antigens specified by Gross leukaemia virus (GLV) the group specific (gs) antigen of C-type RNA murine tumour viruses was demonstrated in FBJ tumours as well as in GLV rat leukaemias, AKR lymphomata and sarcomata induced by MSV-H (Harvey), an MSV isolate of Friend-MoloneyRauscher (FMR) subgroup specificity. Using mouse antisera against antigens present in FBJ cells the Gross (G) or wild type specificity of FBJ tumours was demonstrated by cross reactivity with antigens expressed on normal AKR lymphoid tissues and leukaemias. These antigens were absent from MSV-H induced sarcomata and in reciprocal tests mouse antisera to MSV-H failed to react with antigens present in FBJ tumour cells. No distinction between cellular and virion antigens expressed by FBJ cells was possible by CF although evidence for a cellular antigen with G specificity was obtained in tests using aged C57B1 antiserum containing a naturally occurring G antibody lacking significant virus neutralizing capacity. However, the likelihood that mouse FBJ antisera contain antibodies to type specific viral envelope antigens (VEA) as well as cellular antigen is discussed.

“…Animals and tumours.-The Gross virusinduced lymphoma (C58NT)D (Geering et al, 1966) was maintained in ascitic form by weekly transplantation in weanling syngeneic W/Fu/Ico rats. The G-MuLV-induced lymphoma ESG2 (Old et al, 1965), R-MuLVinduced lymphoma RBL5 (McCoy et al, 1967), Graffi-virus (Gi-MuLV)-induced lymphoma GiL4 (Levy et al, 1968) and benzo(a)-pyrene-induced lymphoma EL4 (Gorer, 1950) were maintained in syngeneic C57BL/6/Ico mice.…”

Section: Methodsmentioning

confidence: 99%

“…Thus, lymphomas induced by the Gross murine leukaemia virus (G-MuLV) express the Gross cell surface antigen (GCSA) which is specific for this MuLV and is not expressed on lymphomas induced by MuLV of the Friend-MoloneyRauscher (FMR) group (Old et al, 1965;Geering et al, 1966). The specificity of GCSA expression can however be questioned in studies of in vitro cultured cells, since in vitro infection of fibroblasts by FMR-MuLV can result in GCSA expression (O'Donnel & Stockert, 1976).…”

Section: Retrovirus-ind Uced) Tumours Bearmentioning

confidence: 99%

“…Since GCSA has been demonstrated to be glycosylated precursors of gag virus proteins (Ledbetter & Nowinski, 1977;Snyder et al, 1977) the comparison of the expression of this cell-surface antigen with the intracellular viral nucleocapside proteins could provide a further insight into the gag gene expression during infection by G-and FMR-MuLV. A specific determination of the level of GCSA expression was therefore developed, using quantitative absorption of the antiGCSAa activity of a W/Fu rat antiserum defined by a cytotoxicity assay on E,G2 lymphoma target cells (Geering et al, 1966, Herberman et al, 1972. GCSAa induction by ecotropic G-MuLV or FMRMuLV and xenotropic murine retroviruses was measured in relation to the level of cytoplasmic viral nucleocapside p30 in the same cells.…”

Section: Retrovirus-ind Uced) Tumours Bearmentioning

confidence: 99%

See 1 more Smart Citation

Measurement of Gross cell-surface antigen and p30 level in murine retrovirus-infected cell lines

Gerlier¹,

Gisselbrecht²,

Guillemain³

et al. 1981

Summary.-The level of Gross cell-surface antigen (GCSAa) expression at the surface of murine retrovirus-infected fibroblasts was determined by quantitative absorption of the anti-GCSAa activity of a serum produced in syngeneic W/Fu rats immunized against (C58NT)D lymphoma, and tested in a cytotoxicity assay against ESG2 lymphoma cells.While GCSAa was specifically expressed on Gross-type virus (G-MuLV)-induced lymphoma cells, and while G-MuLV and G-related MuLV induced a high level of GCSAa expression on murine fibroblasts, the Friend-Moloney-Rauscher (FMR) group viruses (FMR MuLV) and xenotropic isolates were also able to induce a high or intermediate level of GCSAa. Since GCSAa has been shown to be borne by glycosylated precursors of the viral nucleocapside (gp95gag and gp85gag), the amount of GCSAa expressed on these cells was compared to the level of cytoplasmic p30. In G-and G-related MuLV-infected cell lines, a significant relationship was found between the amount of GCSAa and the level of p30, whereas in FMR-MuLV or xenotropic virus-infected cells the amount of GCSAa varied independently of the p30 level. These results could explain the discrepancy in the specificity of expression of GCSAa in vivo and in vitro.