scholarly journals Suppression of endogenous murine leukemia virus by maternal resistance factor.

1983 ◽  
Vol 158 (2) ◽  
pp. 506-514 ◽  
Author(s):  
M Melamedoff ◽  
F Lilly ◽  
M L Duran-Reynals
Keyword(s):  
Murine Leukemia Virus ◽  
Infectious Virus ◽  
Leukemia Virus ◽  
Inbred Mouse ◽  
Resistance Factor ◽  
Mouse Strains ◽  
B Mice ◽  
Akr Mice ◽  
Old Females ◽  
Murine Leukemia

Females of the RF and SJL inbred mouse strains transmit to their progeny of both sexes a nonmendelian maternal resistance factor (MRF) able to suppress the expression of endogenous ecotropic murine leukemia virus (E-MuLV). This MRF is demonstrable in crosses with AKR mice by comparing E-MuLV expression in the spleens and thymuses of reciprocal F1 generations. DBA/2 and ST/b mice are MRF negative by these criteria. Neonatal inoculation of E-MuLV-containing spleen extracts gives rise to persistent expression of infectious virus in mice of the MRF- but not the MRF+ strains. However, inoculation of the virus in 30-d-old females of the MRF- strains no longer leads to a state of persistent infection; instead, these females become MRF+ and transmit protection against E-MuLV expression to their progeny by AKR and RF males. The MRF appears to be transmitted to the progeny mainly through the milk, since foster-nursing AKR neonates on RF (but not DBA/2) mothers greatly reduces E-MuLV expression in the progeny. These RF-fostered AKR mice also show a reduced and delayed lymphoma incidence, a finding consistent with the idea that maternally transmitted resistance to E-MuLV expression is the basis for the classic maternal resistance to lymphomagenesis seen in the progeny of RF mothers.

scholarly journals Amplified env and gag products on AKR cells. Origin from different murine leukemia virus genomes.

1980 ◽  
Vol 151 (4) ◽  
pp. 975-979 ◽  
Author(s):  
J S Tung ◽  
E Fleissner
Keyword(s):  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Mouse Strains ◽  
Type Antigen ◽  
Mink Cell ◽  
Virus Expression ◽  
Virus Genomes ◽  
Akr Mice ◽  
Ecotropic Virus ◽  
Murine Leukemia

Thymocytes of AKR mice express two species of gp70, the envelope glycoprotein of murine leukemia virus (MuLV), encoded by the env gene. One is denoted Ec+ gp70 in reference to the type-antigen Ec and association with ecotropic virus. The other, Ec- gp70, resembles gp70 found also on thymocytes of mouse strains that are not overt producers of MuLV, and has no evident relation to ecotropic virus. Expression of Ec- gp70 type, but not of Ec+ gp70 type, is amplified with age on AKR thymocytes. In contrast, viral core polyproteins, encoded by the gag gene and simultaneously amplified with age, appear to be related to ecotropic virus. These observations imply selective amplification of products of env and gag genes from two sorts of provirus, a phenomenon which may be connected to the dual genetic origin of recombinant mink-cell-focus inducing viruses in AKR mice.

scholarly journals Genetic Regulation of Long-Term Nonprogression in E-55+ Murine Leukemia Virus Infection in Mice

1999 ◽  
Vol 73 (11) ◽  
pp. 9232-9236
Author(s):  
Vily Panoutsakopoulou ◽  
Kathryn Hunter ◽  
Thomas G. Sieck ◽  
Elizabeth P. Blankenhorn ◽  
Kenneth J. Blank
Keyword(s):  
Bone Marrow ◽  
Murine Leukemia Virus ◽  
Genetic Locus ◽  
Leukemia Virus ◽  
Inbred Mouse ◽  
Major Histocompatibility Complex Gene ◽  
Mouse Strains ◽  
Term Survival ◽  
Murine Leukemia

ABSTRACT Certain inbred mouse strains display progression to lymphoma development after infection with E-55+ murine leukemia virus (E-55+ MuLV), while others demonstrate long-term nonprogression. This difference in disease progression occurs despite the fact that E-55+ MuLV causes persistent infection in both immunocompetent BALB/c–H-2k (BALB.K) progressor (P) and C57BL/10–H-2k (B10.BR) long-term nonprogressor (LTNP) mice. In contrast to immunocompetent mice, immunosuppressed mice from both P and LTNP strains develop lymphomas about 2 months after infection, indicating that the LTNP phenotype is determined by the immune response of the infected mouse. In this study, we used bone marrow chimeras to demonstrate that the LTNP phenotype is associated with the genotype of donor bone marrow and not the recipient microenvironment. In addition, we have mapped a genetic locus that may be responsible for the LTNP trait. Microsatellite-based linkage analysis demonstrated that a non-major histocompatibility complex gene on chromosome 15 regulates long-term survival and is located in the same region as the Rfv3 gene. Rfv3 is involved in recovery from Friend virus-induced leukemia and has been demonstrated to regulate neutralizing virus antibody titers. In our studies, however, both P and LTNP strains produce similar titers of neutralizing and cytotoxic anti-E-55+ MuLV. Therefore, while it is possible that Rfv3 influences the course of E-55+ MuLV infection, it is more likely that the LTNP phenotype in E-55+ MuLV-infected mice is regulated by a different, closely linked gene.

scholarly journals QUANTITATIVE STUDIES OF NATURALLY OCCURRING MURINE LEUKEMIA VIRUS INFECTION OF AKR MICE

1972 ◽  
Vol 135 (2) ◽  
pp. 429-436 ◽  
Author(s):  
Wallace P. Rowe ◽  
Theodore Pincus
Keyword(s):  
Virus Infection ◽  
Murine Leukemia Virus ◽  
Infectious Virus ◽  
Leukemia Virus ◽  
Organ Distribution ◽  
Thymic Lymphoma ◽  
Quantitative Studies ◽  
Naturally Occurring ◽  
Akr Mice ◽  
Murine Leukemia

Quantitative studies were made of the organ distribution of murine leukemia virus in AKR mice of various ages. Infectious virus first appeared shortly before or after birth and was continuously present in all mice thereafter. Highest infectivity titers were found in uterus and bone, with spleen slightly lower. Virus titers in normal thymus were relatively low, but increased significantly with the development of thymic lymphoma. The level of viremia decreased after the 1st month of life, but increased sharply in lymphomatous mice.

scholarly journals STUDIES OF GENETIC TRANSMISSION OF MURINE LEUKEMIA VIRUS BY AKR MICE

1972 ◽  
Vol 136 (5) ◽  
pp. 1272-1285 ◽  
Author(s):  
Wallace P. Rowe
Keyword(s):  
Linkage Group ◽  
Murine Leukemia Virus ◽  
Infectious Virus ◽  
Leukemia Virus ◽  
Backcross Generation ◽  
Genetic Transmission ◽  
Group I ◽  
Akr Mice ◽  
Chromosomal Loci ◽  
Murine Leukemia

AKR mice, which regularly contain infectious murine leukemia virus, were mated with four Fv-1n strains of mice which show little or no expression of virus. F1, F2, and first and second backcross generation hybrids were tested for virus in tail tissue at 2 and 6 wk of age. The segregation data indicate that the AKR mouse contains two unlinked, autosomal, chromosomal loci, either of which suffices to induce detectable levels of infectious virus in Fv-1n progeny by 6 wk of age. One of the loci (tentatively referred to as V1) is on linkage group I, 25–30 map units from the locus for albino; the gene order tentatively appears to be N1-c-Hbb.

scholarly journals X-gp70: a third molecular species of the envelope protein gp70 of murine leukemia virus, expressed on mouse lymphoid cells.

1976 ◽  
Vol 143 (4) ◽  
pp. 969-974 ◽  
Author(s):  
J S Tung ◽  
F W Shen ◽  
E Fleissner ◽  
E A Boyse
Keyword(s):  
Molecular Species ◽  
Envelope Protein ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Virus Production ◽  
Lymphoid Cells ◽  
Mouse Strains ◽  
Type Virus ◽  
Murine Leukemia

Three variants of the gp70 envelope component of MuLV are now recognizable serologically: GIX-gp70, 0-gp70, and X-gp70. The last of these, X-gp70, has so far been found only in mice or cells producing abundant C-type virus. This distinguishes X-gp70, provisionally, from the GIX-gp70 and 0-gp70 variants, each of which can be expressed on normal thymocytes without accompanying virus production, as exemplified by mouse strains 129 and B6, respectively. The X-gp70 genotype, however, is not limited to strains of mice-producing abundant virus, because X-gp70+ leukemias occur in strains of mice which do not produce a great deal of virus and whose thymocytes and other tissues are X-gp70-; this is analogous to the appearance of GIX+ leukemias in GIX- mouse strains.

scholarly journals Identification of a new common provirus integration site in gross passage A murine leukemia virus-induced mouse thymoma DNA.

1987 ◽  
Vol 7 (1) ◽  
pp. 512-522 ◽  
Author(s):  
R Villemur ◽  
Y Monczak ◽  
E Rassart ◽  
C Kozak ◽  
P Jolicoeur
Keyword(s):  
T Cell ◽  
Murine Leukemia Virus ◽  
Cell Transformation ◽  
Integration Site ◽  
Leukemia Virus ◽  
Tumor Development ◽  
Mouse Strains ◽  
Mouse Tumor ◽  
Provirus Integration ◽  
Murine Leukemia

The Gross passage A murine leukemia virus (MuLV) induced T-cell leukemia of clonal (or oligoclonal) origin in inoculated mice. To study the role of the integrated proviruses in these tumor cells, we cloned several newly integrated proviruses (with their flanking cellular sequences) from a single tumor in procaryotic vectors. With each of the five clones obtained, a probe was prepared from the cellular sequences flanking the provirus. With one such probe (SS8), we screened several Gross passage A MuLV-induced SIM.S mouse tumor DNAs and found that, in 11 of 40 tumors, a provirus was integrated into a common region designated Gin-1. A 26-kilobase-pair sequence of Gin-1 was cloned from two lambda libraries, and a restriction map was derived. All proviruses were integrated as a cluster in the same orientation within a 5-kilobase-pair region of Gin-1, and most of them had a recombinant structure of the mink cell focus-forming virus type. The frequency of Gin-1 occupancy by provirus was much lower in thymoma induced by other strains of MuLV in other mouse strains. Using somatic-cell hybrid DNAs, we mapped Gin-1 on mouse chromosome 19. Gin-1 was not homologous to 16 known oncogenes and was distinct from the other common regions for provirus integration previously described. Therefore, Gin-1 appears to represent a new common provirus integration region. The integration of a provirus within Gin-1 might be an important event leading to T-cell transformation, and the Gin-1 region might harbor sequences which are involved in tumor development.

scholarly journals AKR Murine Leukemia Virus Genome: Frequency of Sequences in DNA of High-, Low-, and Non-Virus-Yielding Mouse Strains

1974 ◽  
Vol 71 (9) ◽  
pp. 3555-3559 ◽  
Author(s):  
D. R. Lowy ◽  
S. K. Chattopadhyay ◽  
N. M. Teich ◽  
W. P. Rowe ◽  
A. S. Levine
Keyword(s):  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Virus Genome ◽  
Mouse Strains ◽  
Murine Leukemia

Genetic Mapping of a Murine Leukemia Virus-Inducing Locus of AKR Mice

Science ◽  
1972 ◽  
Vol 178 (4063) ◽  
pp. 860-862 ◽  
Author(s):  
W. P. Rowe ◽  
J. W. Hartley ◽  
T. Bremner
Keyword(s):  
Genetic Mapping ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Akr Mice ◽  
Murine Leukemia
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