scholarly journals Spontaneous regression of Friend virus-induced erythroleukemia. I. The role of the helper murine leukemia virus component.

1977 ◽  
Vol 145 (3) ◽  
pp. 594-606 ◽  
Author(s):  
M Dietz ◽  
S P Fouchey ◽  
C Longley ◽  
M A Rich ◽  
P Furmanski
Keyword(s):  
Virus Strain ◽  
Leukemia Virus ◽  
Lymphocytic Leukemia ◽  
Friend Virus ◽  
Newborn Mice ◽  
Icr Mice ◽  
Virus Complex ◽  
Virus Component ◽  
Murine Leukemia

The RFV strain of the Friend virus complex induces an erythroleukemia that spontaneously regresses. The tropism of regressing Friend virus complex (RFV), which is conferred by its helper MuLV component, MuLV-RF, is different from that of the conventional virus strain, CFV. RFV is NB-tropic and CFV is N-tropic. Passage of nonregressing CFV through Fv-1 incompatible Swiss/ICR mice changed the tropism of CFV from N to NB and resulted in a virus strain which induced erythroleukemia that regressed. Passage of NB-tropic CFV back through Fv-1 compatible mice maintained NB-tropism and regression. Altering the quantity or type of helper MuLV in RFV complex by addition of Ri-MuLV inhibited regression in proportion to the amount of added Ri-MuLV. These studies indicate a relationship between a change in virus tropism to NB by passage in certain hosts (e.g., Swiss/ICR mice) and the ability of Friend virus to induce erythroleukemia that spontaneously regresses. MuLV-RF isolated from the RFV complex induced lymphocytic leukemia in newborn mice which regressed and caused the regression of CFV-induced erythroleukemia. MuLV-RF is NB-tropic, contains no spleen focus-forming virus (SFFV) activity and helps SFFV form spleen foci in genetically restrictive mice. Pseudotype viruses were prepared, consisting of MuLV-RF, or other MuLV's, and SFFV derived from FV-B. The pseudotype viruses each acquired the tropism of the MuLV used in rescue. The pseudotype prepared with MuLV-RF or another NB-tropic MuLV-F, but not the virus obtained by rescue with N-tropic MuLV-F, induced erythroleukemia that spontaneously regressed. These studies demonstrate that the ability of RFV to induce erythroleukemia that spontaneously regresses is due to its helper MuLV component.

Spontaneous Regression of Friend Virus-Induced Erythroleukemia. II. Regression of Friend Murine Leukemia Virus-Induced Lymphocytic Leukemia2

1977 ◽  
Vol 59 (3) ◽  
pp. 957-961 ◽  
Author(s):  
Michael Dietz ◽  
Clifford Longley ◽  
Susan P. Fouchey ◽  
LaVonne Hall ◽  
Marvin A. Rich ◽  
...  
Keyword(s):  
Murine Leukemia Virus ◽  
Spontaneous Regression ◽  
Leukemia Virus ◽  
Friend Virus ◽  
Murine Leukemia

scholarly journals Role of intron-contained sequences in formation of moloney murine leukemia virus env mRNA.

1984 ◽  
Vol 4 (11) ◽  
pp. 2289-2297 ◽  
Author(s):  
L S Hwang ◽  
J Park ◽  
E Gilboa
Keyword(s):  
Splice Site ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Splice Junction ◽  
Moloney Murine Leukemia Virus ◽  
Expression Vectors ◽  
Virus Envelope ◽  
Cellular Genes ◽  
Murine Leukemia

Formation of the Moloney murine leukemia virus envelope mRNA involves the removal of a 5,185-base pair-long intron. Deletion analysis of two Moloney murine leukemia virus-derived expression vectors revealed the existence of two short regions within the viral intron which are required for the efficient formation of the spliced RNA species. One region was present upstream from the 3' splice junction, extended at least 85 nucleotides beyond the splice site, and was not more than 165 nucleotides long. As yeast polymerase II introns, the Moloney murine leukemia virus intron contains the sequence 5'-TACTAAC-3' 15 nucleotides upstream from the 3' splice site. A second region located in the middle of the intron, within a 560-nucleotide-long sequence, was also essential for formation of the spliced RNA species. The efficient splicing of the env mRNA in the absence of expression of viral genes raises the possibility that similar mechanisms are used to remove introns of (some) cellular genes.

scholarly journals Thymocyte subsets transformed by Abelson murine leukemia virus.

1985 ◽  
Vol 5 (2) ◽  
pp. 390-397 ◽  
Author(s):  
W D Cook
Keyword(s):  
Cell Lines ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Helper Virus ◽  
Virus Complex ◽  
Blast Cells ◽  
Abelson Murine Leukemia Virus ◽  
Intrathymic Injection ◽  
Abelson Virus ◽  
Murine Leukemia

The infectious complex of Abelson murine leukemia virus was altered by replacing its usual helper virus, Moloney leukemia virus, with radiation leukemia virus (RadLV). After intrathymic injection of the Abelson-RadLV complex, thymomas arose rapidly, as described previously for injection of the Abelson-Moloney complex. Cell lines were derived from thymomas induced by each Abelson virus complex and were classified according to normal thymus cell phenotypes. Each virus complex induced some cell lines which were like a 0.7% subpopulation of murine thymocytes in that they failed to express the Thy-1 cell-surface antigen. These lines are thus far indistinguishable from some Abelson-derived bone marrow transformants classified as pre-B cells. However, the Abelson-Moloney complex induced some cell lines which expressed low levels of Thy-1 and which shared most markers with immature blast cells of the thymic medulla, whereas the Abelson-RadLV complex induced some lines which were clearly like thymic cortex blast cells. Thus, Abelson virus can induce thymoma cell lines of at least two, and possibly three, distinct phenotypes corresponding to normal thymocyte blast subsets, the determination of which can be influenced by helper virus sequences.

scholarly journals Erythroleukemia induction by replication-competent type C viruses cloned from the anemia- and polycythemia-inducing isolates of Friend leukemia virus.

1980 ◽  
Vol 151 (6) ◽  
pp. 1493-1503 ◽  
Author(s):  
M E MacDonald ◽  
T W Mak ◽  
A Bernstein
Keyword(s):  
Leukemia Virus ◽  
Kinetic Studies ◽  
Biological Properties ◽  
Erythroid Cells ◽  
Erythroid Progenitor ◽  
Newborn Mice ◽  
Adult Mice ◽  
Friend Leukemia ◽  
Virus Complex ◽  
Friend Leukemia Virus

In this study, the biological properties of the replication-competent viruses, F-MuLVA, present in the anemia-inducing isolate of Friend leukemia virus complex (FV-A); and F-MuLVP, present in the polycythemia-inducing isolate of Friend leukemia virus complex (FV-P) have been examined. BALB/c mice infected as newborns with clonal isolates of F-MuLVA or F-MuLVP become anemic and show splenic enlargement characterized by an increased proportion of cells that resemble immature nucleated erythroid cells. In addition, the spleens of these F-MuLVA- or F-MuLVP-infected mice contain a markedly increased proportion of both erythropoietin-dependent erythroid progenitor cells and spectrin-containing erythroid cells. These results suggest that Friend murine leukemia virus (F-MuLV) by itself can induce an erythroleukemic transformation in newborn BALB/c mice similar to that induced by the anemia-inducing spleen focus-forming virus (SFFVA) in newborn or adult mice. Kinetic studies indicated that the alterations in hemopoietic cell populations induced by F-MuLVA or F-MuLVP in newborn BALB/c mice occurred more slowly than the rapid changes observed after infection with FV-A. In addition, adult BALB/c mice were fully susceptible to the erythroleukemic transformation induced by either SFFVA or SFFVP, whereas only newborn mice were susceptible to F-MuLV. Taken together, these results suggest that, although the replication-defective Friend spleen focus-forming viruses appear to be the major determinant of erythroleukemia induction in adults, the replication-competent helper F-MuLV also have erythroleukemic potential when assayed in newborn animals.

Sign in / Sign up

Export Citation Format

Share Document