Spleen focus-forming Friend virus: identification of genomic RNA and its relationship to helper virus RNA

Self Cite

105

A series of insertion-deletion mutants was constructed in a molecularly cloned DNA copy of the Friend strain of spleen focus-forming virus (SFFV). The mutants were produced by inserting a synthetic oligonucleotide linker containing the recognition sequence of SalI endonuclease into several different locations of the SFFV DNA. Three classes of mutants were isolated: insertion-deletion mutants in the 5' half of the SFFV genome, in the long terminal repeat of the SFFV genome, and in the env gene of the SFFV genome. The env gene mutant has a deletion of sequences shared in common between the env gene of SFFV and the env genes of mink cell focus-inducing murine leukemia viruses. From analyses of the biological activity of the various mutants and a biologically active subgenomic SFFV DNA fragment described herein, we can deduce that the coding sequence encompassing the env gene of SFFV is required for the biological activity. This region, required for the pathogenic phenotype, cannot be larger than 1.5 kilobase pairs, a size only slightly more than that sufficient to encode the nonglycosylated precursor of the gp52 env gene product.

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Envelope gene sequences which encode the gp52 protein of spleen focus-forming virus are required for the induction of erythroid cell proliferation

Linemeyer¹,

Menke²,

Ruscetti³

et al. 1982

Self Cite

105

“…The polytropic env gene probe was excised from a plasmid containing a 620-bp BamHI-to-EcoRI fragment cloned from a polycythemia-inducing strain of the Friend spleen focusforming virus (35). The defective spleen focus-forming virus corresponds to a deleted polytropic virus (24), and the BamHI-to-EcoRI fragment is homologous to an identically sized fragment in polytropic genomes (see Fig. 6).…”

Section: Methodsmentioning

confidence: 99%

A multistep process of leukemogenesis in Moloney murine leukemia virus-infected mice that is modulated by retroviral pseudotyping and interference

Lavignon

Evans

1996

Mixed retroviral infections frequently exhibit pseudotyping, in which the genome of one virus is packaged in a virion containing SU proteins encoded by another virus. Infection of mice by Moloney murine leukemia virus (M-MuLV), which induces lymphocytic leukemia, results in a mixed viral infection composed of the inoculated ecotropic M-MuLV and polytropic MuLVs generated by recombination of M-MuLV with endogenous retroviral sequences. In this report, we describe pseudotyping which occurred among the polytropic and ecotropic MuLVs in M-MuLV-infected mice. Infectious center assays of polytropic MuLVs released from splenocytes or thymocytes of infected mice revealed that polytropic MuLVs were extensively pseudotyped within ecotropic virions. Late in the preleukemic stage, a dramatic change in the extent of pseudotyping occurred in thymuses. Starting at about 5 weeks, there was an abrupt increase in the number of thymocytes that released nonpseudotyped polytropic viruses. A parallel increase in thymocytes that released ecotropic M-MuLV packaged within polytropic virions was also observed. Analyses of the clonality of preleukemic thymuses and thymomas suggested that the change in pseudotyping characteristics was not the result of the emergence of tumor cells. Examination of mice infected with M-MuLV, Friend erythroleukemia virus, and a Friend erythroleukemia virus-M-MuLV chimeric virus suggested that the appearance of polytropic virions late in the preleukemic stage correlated with the induction of lymphocytic leukemia. We discuss different ways in which pseudotypic mixing may facilitate leukemogenesis, including a model in which the kinetics of thymic infection, modulated by pseudotyping and viral interference, facilitates a stepwise mechanism of leukemogenesis.

“…The discrepancy in 1 2 the extent of homology could be explained by the sensitivity of the method; that is, differences of one or two nucleotides in RNA sequences would be recognized as different spots in fingerprinting analysis, but could be recognized as 1MW related sequences in hybridization studies. This explanation allows the possibility that some !I-~spots recognized as SFFV specific in this manu-34 script may be related, but not identical, to those of FN-2 RNA; this was shown to be the case in a recent paper by Evans et al (8). P…”

Section: Resultsmentioning

confidence: 52%

Analysis of spleen focus-forming virus-specific RNA sequences coding for spleen focus-forming virus-specific glycoprotein with a molecular weight of 55,000 (gp55)

Yoshida¹,

Yasuda²

1980

The 32S RNA of the Friend strain of spleen focus-forming virus (SFFV) contains two sets of sequences: about half is specific to SFFV, and the other half is in common with the sequence of the helper lymphatic leukemia virus. Fingerprinting analysis of RNase T1 oligonucleotides showed that the SFFV-specific sequences were located in two distinct regions: in the 3' half and near the 5' terminus of the genome. Translation of SFFV RNA in a cell-free system yielded three SFFV-specific polypeptides: two main products with molecular weights of about 47,000 (P47) and 16,000 (P16) and a variable amount of a product with a molecular weight of 40,000 (P40). P47 was translated from polyadenylic acidcontaining fragments of 1,500 to 3,000 nucleotides with SFFV-specific sequences from the 3' half of the genome, whereas P16, which contained peptides in common with those of P47, was synthesized by smaller RNA. P47 formed in vitro was found to be structurally related to the protein portion of a glycoprotein, gp55, specifically found in SFFV-infected cells in vivo., It is concluded from the results that a defective env gene containing SFFV-specific sequences in the 3' half of the genome codes for SFFV-specific gp55.