scholarly journals AUTOGENOUS IMMUNITY TO ENDOGENOUS RNA TUMOR VIRUS

1973 ◽  
Vol 138 (1) ◽  
pp. 194-208 ◽  
Author(s):  
J. N. Ihle ◽  
M. Yurconic ◽  
M. G. Hanna
Keyword(s):  
Murine Leukemia Virus ◽  
Gradient Analysis ◽  
Leukemia Virus ◽  
Age Groups ◽  
Rat Serum ◽  
High Incidence ◽  
Tumor Virus ◽  
Akr Mice ◽  
Murine Leukemia ◽  
Precipitation Test

The radioimmune precipitation assay using 3H-labeled AKR leukemia virus was applied to the detection and quantitation of natural serum antibodies directed against endogenous murine leukemia virus (MuLV) envelope antigens B6C3F1 and BALB/c mice, which have low natural incidences of leukemia and lymphoma, and AKR mice, which have a high incidence, were used in this study. Sera from mice of various age groups were assayed. A marked difference in age-associated levels of the autogenous immune response to endogenous murine leukemia virus was detected, and the quantitative differences among these strains were inversely related to the incidence of lymphoma. The radioimmune precipitation test as applied was 500 times more sensitive than virus neutralization. That the reactions we have observed are specific is suggested by several lines of evidence, including the nonreactivity of normal hamster and absorbed rat serum, the positive reaction of absorbed rat anti-AKR serum, the inhibition of precipitation of labeled virus by purified unlabeled virus, and isopycnic gradient analysis of the reactive products.

Immunoferritin Labelling of Murine Leukemia Virus Antigens in thin Sections

1980 ◽  
Vol 38 ◽  
pp. 508-509
Author(s):  
Ray A. Weigand ◽  
Gregory C. Varjabedian
Keyword(s):  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Intracellular Localization ◽  
Uranyl Acetate ◽  
Antibody Technique ◽  
Thin Sections ◽  
Tumor Virus ◽  
Labelling Procedure ◽  
Unlabelled Antibody ◽  
Murine Leukemia

We previously described the intracellular localization of murine mammary tumor virus (MuMTV) p28 protein in thin sections (1). In that study, MuMTV containing cells fixed in 3% paraformaldehyde plus 0.05% glutaraldehyde were labelled after thin sectioning using ferritin-antiferritin in an unlabelled antibody technique. We now describe the labelling of murine leukemia virus (MuLV) particles using the unlabelled antibody technique coupled to ferritin-Fab antiferritin. Cultures of R-MuLV in NIH/3T3 cells were grown to 90% confluence (2), fixed with 2% paraformaldehyde plus 0.5% glutaraldehyde in 0.1 M cacodylate at pH 7.2, postfixed with buffered 17 OsO4, dehydrated with a series of etha-nols, and embedded in Epon. Thin sections were collected on nickel grids, incubated in 107 H2O2, rinsed in HEPES buffered saline, and subjected to the immunoferritin labelling procedure. The procedure included preincubation in 27 egg albumin, a four hour incubation in goat antisera against purified gp69/71 of MuLV (3) (primary antibody), incubation in F(ab’)2 fragments of rabbit antisera to goat IgG (secondary antibody), incubation in apoferritin, incubation in ferritin-Fab ferritin, and a brief fixation with 2% glutaraldehyde. The sections were stained with uranyl acetate and examined in a Siemens IA electron microscope at an accelerating voltage of 60 KV.

scholarly journals A Moloney Murine Leukemia Virus-Based Retrovirus with 4070A Long Terminal Repeat Sequences Induces a High Incidence of Myeloid as Well as Lymphoid Neoplasms

2003 ◽  
Vol 77 (8) ◽  
pp. 4965-4971 ◽  
Author(s):  
Linda Wolff ◽  
Richard Koller ◽  
Xinrong Hu ◽  
Miriam R. Anver
Keyword(s):  
Long Terminal Repeat ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Terminal Repeat ◽  
Moloney Murine Leukemia Virus ◽  
Neoplastic Disease ◽  
Broad Host Range ◽  
Genetically Engineered Mice ◽  
High Incidence ◽  
Murine Leukemia

ABSTRACT Retroviruses can be used to accelerate hematopoietic cancers predisposed to neoplastic disease by prior genetic manipulations such as in transgenic or knockout mice. The virus imparts a second neoplastic “hit,” providing evidence that the initial hit is transforming. In the present study, a unique retrovirus was developed that can induce a high incidence of myeloid disease and has a broad host range. This agent is a Moloney murine leukemia virus (Mo-MuLV)-based virus that has most of the U3 region of the long terminal repeat (LTR) replaced with that of retrovirus 4070A. Like Mo-MuLV, this virus, called MOL4070LTR, is NB-tropic and not restricted by Fv1 allelles. MOL4070LTR causes myeloid leukemias in ca. 50% of mice, a finding in contrast to Mo-MuLV, which induces almost exclusively lymphoid disease. The data suggest that the LTR of the 4070A virus expands the tissue tropism of the disease to the myeloid lineage. Interesting, MCF recombinant envelope was expressed in the lymphoid but not the myeloid neoplasms of BALB/c mice. This retrovirus has the potential for accelerating myeloid disease in genetically engineered mice.

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.

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

scholarly journals Relationship of infectious murine leukemia virus and virus-related antigens in genetic crosses between AKR and the Fv-1 compatible strain C57L.

1976 ◽  
Vol 143 (1) ◽  
pp. 32-46 ◽  
Author(s):  
H Ikeda ◽  
W P Rowe ◽  
E A Boyse ◽  
E Stockert ◽  
H Sato ◽  
...  
Keyword(s):  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Specific Antigen ◽  
Viral Envelope ◽  
Progeny Testing ◽  
Chromosomal Genes ◽  
Relationship Of ◽  
Akr Mice ◽  
Murine Leukemia ◽  
High Output

In a further genetic study of murine leukemia virus (MuLV) and its components we examined the backcross C57L X (C57L X AKR). This population was selected because strains AKR and C57L are both Fv-1n, and the restriction which the Fu-1b allele imposes on the output of virus was thereby obviated. The segregants were scored for three characters: (a) infectious Gross-AKR-type MuLV (V), in the tail; (b) group-specific antigen indicative of p30 internal viral protein, in spleen; and (c) GIX antigen, now thought to be indicative of gp69/71 viral envelope glycoprotein, on thymocytes. Our conclusions are: (a) It is confirmed that the AKR mouse has two unlinked chromosomal genes, Akv-1 and Akv-2, each of which can independently give rise to the life-long high output of MuLV that is characteristic of AKR mice. (b) Of the eight phenotypes that could possibly be derived from segregation of the three pairs of independent alternative traits, seven were observed, but on progeny testing only three were shown to reflect stably heritable genotypes; these were V+p30+GIX+ and V-p30-GIX- (the parental types) and V-p30+GIX+. A third, newly identified AKR gene, designated Akvp, segregating independently of Akv-1 and Akv-2, also determines expression of p30 and GIX but in this case independently of XC-detectable MuLV. (c) The four remaining observed phenotypes, which did not breed true on progeny testing, involved mostly antigen-negative parents yielding antigen-positive progeny; it is likely that these discrepancies represented suppression of phenotype by a maternal resistance factor.

Immunologic Localization of Murine Leukemia Virus Antigens in Thin Sections

1981 ◽  
Vol 39 ◽  
pp. 402-403
Author(s):  
Ray A. Weigand ◽  
Carol I. Paquette ◽  
Clifford Longley ◽  
Philip Furmanski
Keyword(s):  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Intracellular Localization ◽  
Protein A ◽  
Thin Sections ◽  
Virus Particles ◽  
Tumor Virus ◽  
Labelling Procedure ◽  
Nih 3T3 ◽  
Murine Leukemia

In order to examine the temporal sequence of intracellular events which culminates in the release of infectious virus particles from the cell surface, we have developed immunoferritin techniques to localize viral antigens in thin sections. We previously described the intracellular localization of murine mammary tumor virus p28 protein in thin sections using an unlabelled antibody procedure with ferritin-antiferritin. We now describe the labelling of murine leukemia virus (MuLV) in thin sections using anti-MuLV and Protein A-ferritin.Cultures of F-MuLV in NIH/3T3 cells were grown to 90% confluence, fixed, dehydrated, and embedded in Epon as before. Thin sections were picked up on nickel grids, incubated in 20% H2O2 for 20 min, rinsed in PBS, and subjected to the labelling procedure. The labelling protocol included: preincubation in 5% BSA in PBS, rinse in 1% BSA in PBS, 3 hour incubation in rabbit anti-MuLV, rinse in 1% BSA in PBS, incubation in apoferritin, incubation in Protein A-ferritin (Zymed Labs., Burlingame, CA), rinses in 1% BSA in PBS and PBS, and incubation in 2% glutaraldehyde in PBS.

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.

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