Rauscher Spleen Focus-forming Virus: Biological Properties and Relationship to Helper Viruses

Mol, J.A.; Ostertag, Wolfram; Bilello, J. A.; Stoof, T.J.

doi:10.1099/0022-1317-63-1-45

Cited by 10 publications

(19 citation statements)

References 29 publications

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“…They also appear to have defects in the viral gene. The non-producer lines obtained by Anand et al (1981 b) appear to have a defect in the expression of the 5' portion of the helper viral genome, and non-producer lines derived from a Rauscher virus-transformed erythroid cell line could be superinfected with Friend, Moloney and Gross viruses (Mol et al, 1982). However, the genetic defects in our mutants appear to be different from these non-producers.…”

Section: Short Communicationmentioning

confidence: 54%

Friend Erythroleukaemia Cell Mutants Defective in Viral Gene Expression

Yokota

Iwamoto

Suzuki

et al. 1984

Journal of General Virology

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SUMMARYCellular mutants defective in the expression of viral polypeptides were isolated from the Friend erythroleukaemia cell line 745a by immunoselection with anti-ecotropic murine leukaemia virus serum in the presence of complement. The mode of appearance of the antiserum-resistant cells showed an interesting pattern which is discussed in the text. One of the mutants obtained contained no detectable gp70 or pl5(E) while retaining gPr90 env; defects appeared to reside in the processing of the gPr90 env to gp70 and pl5(E). In another type of mutant, gPr90 env was not detected. All these mutants retained spleen focus-forming virus (SFFV)-specific gp55 and gag precursor Pr68 gag. The mutants superinfected with the helper virus produced the helper and SFFV also, indicating that these mutations did not affect the replication of the exogenously infecting virus.

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Section: Short Communicationmentioning

confidence: 54%

Friend Erythroleukaemia Cell Mutants Defective in Viral Gene Expression

Yokota

Iwamoto

Suzuki

et al. 1984

Journal of General Virology

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“…The oligonucleotide pattern of the latter is presented in Fig. 1 and shows a similar stoichiometry to the pattern of 3T3 clone 9 (Mol et al, 1982). It seems likely, therefore, that cloning in vivo has taken place by serial transfer.…”

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confidence: 72%

“…The cloned virus was called 3T3-R-MuLV clone 9 and was XC-positive and consisted of only the 35S RNA component. The oligonucleotide pattern was homogeneous and all spots showed a similar labelling density due to a stoichiometric distribution (Mol et al, 1982). Injection of this cloned virus into newborn mice resulted in a lymphatic leukaemia in 75 % of the animals.…”

mentioning

confidence: 85%

“…This virus has been shown to be heterogeneous in RNA composition (Mol et al, 1982). From this viral preparation the eeotropic helper virus was cloned by endpoint dilution and infection of 3T3 cells.…”

mentioning

confidence: 99%

“…Also, the virus from the serum of an infected C57/Black mouse 0000-6299 © 1985 SGM (Wright & Lasfarques, 1965). From this viral complex the ecotropic lymphatic leukaemia helper virus was cloned by endpoint dilution and infection of BALB/c 3T3 or NIH 3T3 cells (clone 9) (Mol et al, 1982). Other viral preparations originated from sera of infected mice, which showed an overt lymphatic or myeloid leukaemia.…”

mentioning

confidence: 99%

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The Induction of Myeloid Leukaemias by Rauscher Murine Leukaemia Virus

Both¹,

Stoof²,

Kranendonk³

et al. 1985

Journal of General Virology

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Syngeneic monoclonal antibodies directed against rauscher virusinduced myeloid leukemic cells: Isolation and characterization

Berends

Rhijnsburger

Gaalen

et al. 1988

Intl Journal of Cancer

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Hybridomas producing syngeneic monoclonal antibodies (MAbs) were prepared by fusion of spleen cells of BALB/c mice, which were immunized with sublethal doses of RMB-I cells. This cell line originates from a Rauscher virus (R-MuLV)-induced myeloid leukemia and forms tumors when re-inoculated into mice. MAbs were characterized as regards their reactivity against virally and non-virally induced cell lines. Two selected MAbs, IC5F5 and 4D2B4, were analyzed further. Their binding to subcellular structures was determined, and so were the properties of the antigens to which they are directed. MAb IC5F5 is of the IgG2A and 4D2B4 of the IgG2b subclass. Both bind to R-MuLV-infected or -transformed cell lines and are not mutually competitive. The antibodies do not react with other murine and human myeloid leukemic cells. As shown by immuno-electron microscopy, these MAbs have affinity to the cell membrane of non-virus producing RMB-I cells. When lysates of purified virus were analyzed, the MAbs were found to be directed to the gag precursor protein Pr65, and one of them (IC5F5) also to be directed to the core protein p12. In RMB-I cells, binding occurs to a 50-kDa glycoprotein and 2 proteins of 26 and 29 kDa. Since RMB-I cells do not produce virus, but express aberrant viral proteins, these MAbs are tumor-specific and useful for immunotherapy.

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Rauscher Spleen Focus-forming Virus: Biological Properties and Relationship to Helper Viruses

Cited by 10 publications

References 29 publications

Friend Erythroleukaemia Cell Mutants Defective in Viral Gene Expression

Friend Erythroleukaemia Cell Mutants Defective in Viral Gene Expression

The Induction of Myeloid Leukaemias by Rauscher Murine Leukaemia Virus

Syngeneic monoclonal antibodies directed against rauscher virusinduced myeloid leukemic cells: Isolation and characterization

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