A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) isolated from spontaneous leukemia in AKR strain mice.
Species of GAMMARETROVIRUS, containing many well-defined strains, producing leukemia in mice. Disease is commonly induced by injecting filtrates of propagable tumors into newborn mice.
Inbred AKR mice are a strain of laboratory mice that are homozygous at all gene loci and have a high incidence of developing certain diseases, such as leukemia and autoimmune disorders, making them useful for research purposes in biomedicine.
A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) arising during the propagation of S37 mouse sarcoma, and causing lymphoid leukemia in mice. It also infects rats and newborn hamsters. It is apparently transmitted to embryos in utero and to newborns through mother's milk.
A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) producing leukemia of the reticulum-cell type with massive infiltration of liver, spleen, and bone marrow. It infects DBA/2 and Swiss mice.
Leukemia induced experimentally in animals by exposure to leukemogenic agents, such as VIRUSES; RADIATION; or by TRANSPLANTATION of leukemic tissues.
A replication-defective strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) capable of transforming lymphoid cells and producing a rapidly progressing lymphoid leukemia after superinfection with FRIEND MURINE LEUKEMIA VIRUS; MOLONEY MURINE LEUKEMIA VIRUS; or RAUSCHER VIRUS.
A species of GAMMARETROVIRUS causing leukemia, lymphosarcoma, immune deficiency, or other degenerative diseases in cats. Several cellular oncogenes confer on FeLV the ability to induce sarcomas (see also SARCOMA VIRUSES, FELINE).
A strain of MURINE LEUKEMIA VIRUS associated with mouse tumors similar to those caused by the FRIEND MURINE LEUKEMIA VIRUS. It is a replication-competent murine leukemia virus. It can act as a helper virus when complexing with a defective transforming component, RAUSCHER SPLEEN FOCUS-FORMING VIRUS.
Virus diseases caused by the RETROVIRIDAE.
The type species of DELTARETROVIRUS that causes a form of bovine lymphosarcoma (ENZOOTIC BOVINE LEUKOSIS) or persistent lymphocytosis.
A progressive, malignant disease of the blood-forming organs, characterized by distorted proliferation and development of leukocytes and their precursors in the blood and bone marrow. Leukemias were originally termed acute or chronic based on life expectancy but now are classified according to cellular maturity. Acute leukemias consist of predominately immature cells; chronic leukemias are composed of more mature cells. (From The Merck Manual, 2006)
Family of RNA viruses that infects birds and mammals and encodes the enzyme reverse transcriptase. The family contains seven genera: DELTARETROVIRUS; LENTIVIRUS; RETROVIRUSES TYPE B, MAMMALIAN; ALPHARETROVIRUS; GAMMARETROVIRUS; RETROVIRUSES TYPE D; and SPUMAVIRUS. A key feature of retrovirus biology is the synthesis of a DNA copy of the genome which is integrated into cellular DNA. After integration it is sometimes not expressed but maintained in a latent state (PROVIRUSES).
Established cell cultures that have the potential to propagate indefinitely.
The process of intracellular viral multiplication, consisting of the synthesis of PROTEINS; NUCLEIC ACIDS; and sometimes LIPIDS, and their assembly into a new infectious particle.
Strains of MURINE LEUKEMIA VIRUS discovered in 1976 by Hartley, Wolford, Old, and Rowe and so named because the viruses originally isolated had the capacity to transform cell foci in mink cell cultures. MCF viruses are generated by recombination with ecotropic murine leukemia viruses including AKR, Friend, Moloney, and Rauscher, causing ERYTHROLEUKEMIA and severe anemia in mice.
Deoxyribonucleic acid that makes up the genetic material of viruses.
The functional hereditary units of VIRUSES.
An enzyme that synthesizes DNA on an RNA template. It is encoded by the pol gene of retroviruses and by certain retrovirus-like elements. EC 2.7.7.49.
Specific molecular components of the cell capable of recognizing and interacting with a virus, and which, after binding it, are capable of generating some signal that initiates the chain of events leading to the biological response.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Duplex DNA sequences in eukaryotic chromosomes, corresponding to the genome of a virus, that are transmitted from one cell generation to the next without causing lysis of the host. Proviruses are often associated with neoplastic cell transformation and are key features of retrovirus biology.
Proteins coded by the retroviral gag gene. The products are usually synthesized as protein precursors or POLYPROTEINS, which are then cleaved by viral proteases to yield the final products. Many of the final products are associated with the nucleoprotein core of the virion. gag is short for group-specific antigen.
Infections produced by oncogenic viruses. The infections caused by DNA viruses are less numerous but more diverse than those caused by the RNA oncogenic viruses.
A genus of RETROVIRIDAE comprising endogenous sequences in mammals, related RETICULOENDOTHELIOSIS VIRUSES, AVIAN, and a reptilian virus. Many species contain oncogenes and cause leukemias and sarcomas.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Clonal expansion of myeloid blasts in bone marrow, blood, and other tissue. Myeloid leukemias develop from changes in cells that normally produce NEUTROPHILS; BASOPHILS; EOSINOPHILS; and MONOCYTES.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations, or by parent x offspring matings carried out with certain restrictions. All animals within an inbred strain trace back to a common ancestor in the twentieth generation.
Insertion of viral DNA into host-cell DNA. This includes integration of phage DNA into bacterial DNA; (LYSOGENY); to form a PROPHAGE or integration of retroviral DNA into cellular DNA to form a PROVIRUS.
A species of GAMMARETROVIRUS causing leukemia in the gibbon ape. Natural transmission is by contact.

Adoptive immunotherapy of a Gross virus producing lymphoma and a methylcholanthrene-induced fibrosarcoma in tolerant rats. (1/181)

Immunological tolerance to Gross virus-specific transplantation antigens in rats given neonatae transfer of donor lymphoid cells beneath the kidney capsule of syngeneic recipient rats. Immune or normal donor cells invariably developed a cell-mediated immune reaction in kidneys of GV-tolerant recipients, presumably against GV antigens present on the surface of recipient lymphoid cells in the kidney. Spleen and lymph node cells from tolerant rats failed to develop a reaction in tolerant recipients, but developed a strong reaction to histoincompatible antigens in the kidneys of semisyngeneic tolerant rats. The immunologically tolerant state in the rats could be broken by adoptive transfer of spleen and lymph node cells from syngeneic rats immunized with GV-induced lymphoma cells. Immunotherapy of a GV-induced and also a GV-infected methylcholanthrene-induced fibrosarcoma growing in tolerant rats was successful when immune spleen and lymph node cells were administered i.p. 3 days after s.c. inoculation of 2 X 10(7) tumor cells in the case of the lymphoma, and 1 day after inoculation of 5 X 10(6) tumor cells in the case of the fibrosarcoma.  (+info)

Antiretroviral cytolytic T-lymphocyte nonresponsiveness: FasL/Fas-mediated inhibition of CD4(+) and CD8(+) antiviral T cells by viral antigen-positive veto cells. (2/181)

C57BL/6 (H-2(b)) mice generate type-specific cytolytic T-lymphocyte (CTL) responses to an immunodominant Kb-restricted epitope, KSPWFTTL located in the membrane-spanning domain of p15TM of AKR/Gross murine leukemia viruses (MuLV). AKR.H-2(b) congenic mice, although carrying the responder H-2(b) major histocompatibility complex (MHC) haplotype, are low responders or nonresponders for AKR/Gross MuLV-specific CTL, apparently due to the presence of inhibitory AKR. H-2(b) cells. Despite their expression of viral antigens and Kb, untreated viable AKR.H-2(b) spleen cells cause dramatic inhibition of the C57BL/6 (B6) antiviral CTL response to in vitro stimulation with AKR/Gross MuLV-induced tumor cells. This inhibition is specific (AKR.H-2(b) modulator spleen cells do not inhibit allogeneic MHC or minor histocompatibility antigen-specific CTL production), dependent on direct contact of AKR.H-2(b) cells in a dose-dependent manner with the responder cell population, and not due to soluble factors. Here, the mechanism of inhibition of the antiviral CTL response is shown to depend on Fas/Fas-ligand interactions, implying an apoptotic effect on B6 responder cells. Although B6.gld (FasL-) responders were as sensitive to inhibition by AKR.H-2(b) modulator cells as were B6 responders, B6.lpr (Fas-) responders were largely insensitive to inhibition, indicating that the responder cells needed to express Fas. A Fas-Ig fusion protein, when added to the in vitro CTL stimulation cultures, relieved the inhibition caused by the AKR.H-2(b) cells if the primed responders were from either B6 or B6.gld mice, indicating that the inhibitory AKR.H-2(b) cells express FasL. Because of the antigen specificity of the inhibition, these results collectively implicate a FasL/Fas interaction mechanism: viral antigen-positive AKR.H-2(b) cells expressing FasL inhibit antiviral T cells ("veto" them) when the AKR.H-2(b) cells are recognized. Consistent with this model, inhibition by AKR.H-2(b) modulator cells was MHC restricted, and resulted in approximately a 10- to 70-fold decrease in the in vitro expansion of pCTL/CTL. Both CD8(+) CTL and CD4(+) Th responder cells were susceptible to inhibition by FasL+ AKR.H-2(b) inhibitory cells as the basis for inhibition. The CTL response in the presence of inhibitory cells could be restored by several cytokines or agents that have been shown by others to interfere with activation-induced cell death (e.g. , interleukin-2 [IL-2], IL-15, transforming growth factor beta, lipopolysaccharide, 9-cis-retinoic acid) but not others (e.g., tumor necrosis factor alpha). These results raise the possibility that this type of inhibitory mechanism is generalized as a common strategy for retrovirus infected cells to evade immune T-cell recognition.  (+info)

Definitive evidence that the murine C-type virus inducing locus Akv-1 is viral genetic material. (3/181)

DNA of the AKR mouse contains a set of murine leukemia virus sequences that are not present in DNA of the NIH Swiss mouse. NIH mice partially congenic for the AKR murine-leukemia-virus-inducing locus Akv-1 contain this set of sequences, and, in a three-point cross segregating for Akv-1 on an NIH background, the sequences segregated with Akv-1. It is concluded that the Akv-1 locus contains viral sequences.  (+info)

Mutations of the kissing-loop dimerization sequence influence the site specificity of murine leukemia virus recombination in vivo. (4/181)

The genetic information of retroviruses is retained within a dimeric RNA genome held together by intermolecular RNA-RNA interactions near the 5' ends. Coencapsidation of retrovirus-derived RNA molecules allows frequent template switching of the virus-encoded reverse transcriptase during DNA synthesis in newly infected cells. We have previously shown that template shifts within the 5' leader of murine leukemia viruses occur preferentially within the kissing stem-loop motif, a cis element crucial for in vitro RNA dimer formation. By use of a forced recombination approach based on single-cycle transfer of Akv murine leukemia virus-based vectors harboring defective primer binding site sequences, we now report that modifications of the kissing-loop structure, ranging from a deletion of the entire sequence to introduction of a single point mutation in the loop motif, significantly disturb site specificity of recombination within the highly structured 5' leader region. In addition, we find that an intact kissing-loop sequence favors optimal RNA encapsidation and vector transduction. Our data are consistent with the kissing-loop dimerization model and suggest that a direct intermolecular RNA-RNA interaction, here mediated by palindromic loop sequences within the mature genomic RNA dimer, facilitates hotspot template switching during retroviral cDNA synthesis in vivo.  (+info)

Radioimmunoassay for intact Gross mouse leukemia virus. (5/181)

A radioimmunoassay for intact Gross leukemia virus has been developed using 125I-labeled Gross virus grown in tissue culture and guinea pig antisera to Gross virus grown either in tissue culture or harvested from leukemic C3H(f) mice. Separation of bound from free labeled virus was effected using the double antibody method. The assay can detect fewer than 10(8) virus particles and has been used to measure the viral content of individual organs from inoculated leukemic C3H(f) mice and from Ak mice with spontaneous leukemia. Organs from noninoculated healthy C3H(f) mice crossreacted poorly in the system, virus generally being detectable only in the thymus and spleen and at low concentration. In some of the inoculated C3H(f) leukemic mice the viral content of as little as 0.5 mul of plasma is measurable. That this assay is for intact virus and not for soluble antigens of the viral envelope was proven by the observation that the immunoreactive material of plasma and extracts from thymus and liver of leukemic mice has a buoyant denisty in sucrose of 1.17-1.18 g/ml, corresponding to that of intact virus grown in tissue culture. With this sensitivity it may now be possible to quantitate viral concentrations in tissue and body fluids from the time of inoculation through the development of obvious pathology.  (+info)

Treatment of spontaneous leukemia in AKR mice with chemotherapy, immunotherapy, or interferon. (6/181)

AKR mice are genetically destined to develop Gross (RNA) virus-induced lymphatic leukemia. Leukemic AKR mice treated with combination vincristine, cyclophosphamide (Cytoxan), and 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea sustained a 180% increase of life-span. Combination chemotherapy plus immunization with neuraminidase-treated allogeneic (Gross virus-induced) G2G leukemic cells intradermally resulted in 35% of animals surviving beyond 150 days without evidence of the disease. It is significant that allogeneic E2G leukemic cells as immunogen were as effective in prolonging the life-span of the immunized leukemic AKR mice as were syngeneic leukemic thymocytes. Virazole (1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide), an antiviral compound, alone showed no apparent antitumor effect. However, in experiments in which the clinically diagnosed leukemic AKR mice received a combination of cytoreductive therapy [vincristine plus prednisone or, more effectively, vincristine, Cytoxan plus 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea, followed by Virazole], there was a noticeable reduction of the viral titer, a delay in the reappearance of viable clonogenic cells, and an increase in the survival time for the leukemic AKR mice as compared to those receiving cytoreductive therapy alone. The effectiveness of purified mouse interferon in AKR mice was also examined. The decrease in the viral titer of animals that received interferon treatment was markedly greater than of those receiving a combination of cytoreductive therapy with Virazole or immunotherapy. The administration of mouse interferon had a direct effect on the appearance of the spontaneous leukemia in AKR mice. The median life-span of the control animals was 36 weeks, whereas 45% of the AKR mice treated with five doses of 5 X 10(4) units of interferon are still alive at 54 weeks of age. Thus, interferon not only reduces the Gross murine leukemia virus titer in the chronically infected AKR mice but also significantly delays the appearance of the primary lymphoma.  (+info)

The generation and specificity of cytotoxic T cells raised against syngeneic tumor cells bearing AKR/Gross murine leukemia virus antigens. (7/181)

Efforts were made to generate C57BL/6 cytotoxic effector cells to a syngeneic leukemia (E{male}G2) bearing AKR/Gross virus antigens. As we were unable to induce significant cytotoxic activity by immunization with up to 10(8) irradiated E{male}G2 cells, even when cells from such primed animals were subsequently restimulated with E{male}G2 cells in vitro, C57BL/6 mice were immunized with an aliogeneic, virus-producing AKR leukemic cell line (AKR SL3). Peritoneal exudate cells and, to a lesser degree, spleen cells from these mice showed significant lytic activity toward the immunizing allogeneic tumor but not toward E{male}G2. When spleen cells were harvested from animals {approximately equal to}10 d after injection of AKR SL3 and rechallenged in vitro with either E{male}G2 or AKR.H-2(b) SL1, another tumor that displays AKR/Gross virus antigens, then a vigorous cytotoxic response against E{male}G2 and AKR. H-2(b) SL1 was obtained. Effector cells generated by AKR SL3 priming followed by in vitro stimulation with E{male}G2 or AKR.H-2(b) SL1 lysed only cells of H-2(b) haplotype which were strongly positive for the display of serologically detectable AKR/Gross virus antigens. Thus, AKR SL3 cells were not lysed nor were EL4 cells (H-2(b); but only weakly positive for gp70). Cells not bearing the MuLV antigens tested for, such as P815 mastocytoma cells and spleen cell "blasts" from C57BL/6 and CBA (H-2(k)) mice, were also insusceptible to attack. The cytotoxic effector cells induced bore Thy 1.2 alloantigen and were of the Lyt 1+2+ phenotype. Collectively, these findings are consistent with the conclusion that the cytotoxic T cells raised against E{male}G2 are directed against AKR/Gross virus-associated antigens and are H-2 restricted. It will be of interest to determine the relevance of such effector cells to the known resistance of the C57BL/6 mouse to AKR/Gross virus-induced leukemia.  (+info)

The role of serum factors in the acceleration by Freund's complete adjuvant of the growth of transplanted murine leukemic cells. (8/181)

Attempted nonspecific immunotherapy led to acceleration rather than retardation of tumor growth. Mice given injections of Freund's adjuvant were more susceptible to transplanted syngeneic Gross virus-induced leukemic cells when Freund's complete adjuvant was administered i.p. 0 to 7 days before or 1 day after tumor; thereafter, the adjuvant had no effect. Two serum-mediated phenomeana were demonstrated in vitro: (a) sera from mice immunized with Freund's complete adjuvant and tumor facilitated killing of tumor cells by peritoneal exudate cells from nonimmune mice; (b) sera from all mice with progressive tumor blocked the cytotoxicity of a xenogeneic tumor-specific serum. Certain sera produced both effects. However, sera that either blocked or facilitated tumor killing in vitro had no effect on the growth in vivo of transplanted tumor cells.  (+info)

The AKR murine leukemia virus (AKR MLV) is a type of retrovirus that naturally infects mice of the AKR strain. It is a member of the gammaretrovirus genus and is closely related to other murine leukemia viruses (MLVs).

AKR MLV is transmitted horizontally through close contact with infected animals, as well as vertically from mother to offspring. The virus primarily infects hematopoietic cells, including lymphocytes and macrophages, and can cause a variety of diseases, most notably leukemia and lymphoma.

The AKR MLV genome contains three main structural genes: gag, pol, and env, which encode the viral matrix, capsid, nucleocapsid, reverse transcriptase, integrase, and envelope proteins, respectively. Additionally, the virus carries accessory genes, such as rex and sor, that play a role in regulating viral gene expression and replication.

AKR MLV has been extensively studied as a model system for retrovirus biology and pathogenesis, and its study has contributed significantly to our understanding of the mechanisms of retroviral infection, replication, and disease.

Medical Definition:

Murine leukemia virus (MLV) is a type of retrovirus that primarily infects and causes various types of malignancies such as leukemias and lymphomas in mice. It is a complex genus of viruses, with many strains showing different pathogenic properties.

MLV contains two identical single-stranded RNA genomes and has the ability to reverse transcribe its RNA into DNA upon infection, integrating this proviral DNA into the host cell's genome. This is facilitated by an enzyme called reverse transcriptase, which MLV carries within its viral particle.

The virus can be horizontally transmitted between mice through close contact with infected saliva, urine, or milk. Vertical transmission from mother to offspring can also occur either in-utero or through the ingestion of infected breast milk.

MLV has been extensively studied as a model system for retroviral pathogenesis and tumorigenesis, contributing significantly to our understanding of oncogenes and their role in cancer development. It's important to note that Murine Leukemia Virus does not infect humans.

'Inbred AKR mice' is a strain of laboratory mice used in biomedical research. The 'AKR' designation stands for "Akita Radioactive," referring to the location where this strain was first developed in Akita, Japan. These mice are inbred, meaning that they have been produced by many generations of brother-sister matings, resulting in a genetically homogeneous population with minimal genetic variation.

Inbred AKR mice are known for their susceptibility to certain types of leukemia and lymphoma, making them valuable models for studying these diseases and testing potential therapies. They also develop age-related cataracts and have a higher incidence of diabetes than some other strains.

It is important to note that while inbred AKR mice are widely used in research, their genetic uniformity may limit the applicability of findings to more genetically diverse human populations.

The Moloney murine leukemia virus (Mo-MLV) is a type of retrovirus, specifically a gammaretrovirus, that is commonly found in mice. It was first discovered and isolated by John Moloney in 1960. Mo-MLV is known to cause various types of cancerous conditions, particularly leukemia, in susceptible mouse strains.

Mo-MLV has a single-stranded RNA genome that is reverse transcribed into double-stranded DNA upon infection of the host cell. This viral DNA then integrates into the host's genome and utilizes the host's cellular machinery to produce new virus particles. The Mo-MLV genome encodes for several viral proteins, including gag (group-specific antigen), pol (polymerase), and env (envelope) proteins, which are essential for the replication cycle of the virus.

Mo-MLV is widely used in laboratory research as a model retrovirus to study various aspects of viral replication, gene therapy, and oncogenesis. It has also been engineered as a vector for gene delivery applications due to its ability to efficiently integrate into the host genome and deliver large DNA sequences. However, it is important to note that Mo-MLV and other retroviruses have the potential to cause insertional mutagenesis, which can lead to unintended genetic alterations and adverse effects in some cases.

Friend murine leukemia virus (F-MuLV) is a type of retrovirus that specifically infects mice. It was first discovered by Charlotte Friend in the 1950s and has since been widely used as a model system to study retroviral pathogenesis, oncogenesis, and immune responses.

F-MuLV is a complex retrovirus that contains several accessory genes, including gag, pol, env, and others. The virus can cause leukemia and other malignancies in susceptible mice, particularly when it is transmitted from mother to offspring through the milk.

The virus is also known to induce immunosuppression, which makes infected mice more susceptible to other infections and diseases. F-MuLV has been used extensively in laboratory research to investigate various aspects of retroviral biology, including viral entry, replication, gene expression, and host immune responses.

It is important to note that Friend murine leukemia virus only infects mice and is not known to cause any disease in humans or other animals.

Experimental leukemia refers to the stage of research or clinical trials where new therapies, treatments, or diagnostic methods are being studied for leukemia. Leukemia is a type of cancer that affects the blood and bone marrow, leading to an overproduction of abnormal white blood cells.

In the experimental stage, researchers investigate various aspects of leukemia, such as its causes, progression, and potential treatments. They may conduct laboratory studies using cell cultures or animal models to understand the disease better and test new therapeutic approaches. Additionally, clinical trials may be conducted to evaluate the safety and efficacy of novel treatments in human patients with leukemia.

Experimental research in leukemia is crucial for advancing our understanding of the disease and developing more effective treatment strategies. It involves a rigorous and systematic process that adheres to ethical guidelines and scientific standards to ensure the validity and reliability of the findings.

The Abelson murine leukemia virus (Abelson murine leukemia virus, or A-MuLV) is a type of retrovirus that can cause cancer in mice. It was first discovered in 1970 and has since been widely studied as a model system for understanding the mechanisms of retroviral infection and cancer development.

A-MuLV is named after Peter Nowell and David A. Harrison, who first described the virus and its ability to cause leukemia in mice. The virus contains an oncogene called "v-abl," which encodes a tyrosine kinase enzyme that can activate various signaling pathways involved in cell growth and division. When the v-abl oncogene is integrated into the genome of an infected mouse cell, it can cause uncontrolled cell growth and division, leading to the development of leukemia.

A-MuLV has been used extensively in laboratory research to study the molecular mechanisms of cancer development and to develop new therapies for treating cancer. It has also been used as a tool for introducing specific genetic modifications into mouse cells, allowing researchers to study the effects of those modifications on cell behavior and function.

Feline Leukemia Virus (FeLV) is a retrovirus that primarily infects cats, causing a variety of diseases and disorders. It is the causative agent of feline leukemia, a name given to a syndrome characterized by a variety of symptoms such as lymphoma (cancer of the lymphatic system), anemia, immunosuppression, and reproductive disorders. FeLV is typically transmitted through close contact with infected cats, such as through saliva, nasal secretions, urine, and milk. It can also be spread through shared litter boxes and feeding dishes.

FeLV infects cells of the immune system, leading to a weakened immune response and making the cat more susceptible to other infections. The virus can also integrate its genetic material into the host's DNA, potentially causing cancerous changes in infected cells. FeLV is a significant health concern for cats, particularly those that are exposed to outdoor environments or come into contact with other cats. Vaccination and regular veterinary care can help protect cats from this virus.

I'm sorry for any confusion, but there seems to be no established medical definition or recognition of a "Rauscher Virus" in human or veterinary medicine. It is possible that you may have misspelled or misremembered the name of a specific virus or medical term. If you have more information or context about where this term was used, I'd be happy to help you further research the topic.

Retroviridae infections refer to diseases caused by retroviruses, which are a type of virus that integrates its genetic material into the DNA of the host cell. This allows the virus to co-opt the cell's own machinery to produce new viral particles and infect other cells.

Some well-known retroviruses include human immunodeficiency virus (HIV), which causes AIDS, and human T-lymphotropic virus (HTLV), which can cause certain types of cancer and neurological disorders.

Retroviral infections can have a range of clinical manifestations depending on the specific virus and the host's immune response. HIV infection, for example, is characterized by progressive immunodeficiency that makes the infected individual susceptible to a wide range of opportunistic infections and cancers. HTLV infection, on the other hand, can cause adult T-cell leukemia/lymphoma or tropical spastic paraparesis, a neurological disorder.

Prevention and treatment strategies for retroviral infections depend on the specific virus but may include antiretroviral therapy (ART), vaccination, and behavioral modifications to reduce transmission risk.

Bovine Leukemia Virus (BLV) is a retrovirus that infects cattle and causes enzootic bovine leukosis, a neoplastic disease characterized by the proliferation of malignant B-lymphocytes. The virus primarily targets the animal's immune system, leading to a decrease in the number of white blood cells (leukopenia) and an increased susceptibility to other infections.

The virus is transmitted horizontally through close contact with infected animals or vertically from mother to offspring via infected milk or colostrum. The majority of BLV-infected cattle remain asymptomatic carriers, but a small percentage develop clinical signs such as lymphoma, weight loss, and decreased milk production.

BLV is closely related to human T-cell leukemia virus (HTLV), and both viruses belong to the Retroviridae family, genus Deltaretrovirus. However, it's important to note that BLV does not cause leukemia or any other neoplastic diseases in humans.

Leukemia is a type of cancer that originates from the bone marrow - the soft, inner part of certain bones where new blood cells are made. It is characterized by an abnormal production of white blood cells, known as leukocytes or blasts. These abnormal cells accumulate in the bone marrow and interfere with the production of normal blood cells, leading to a decrease in red blood cells (anemia), platelets (thrombocytopenia), and healthy white blood cells (leukopenia).

There are several types of leukemia, classified based on the specific type of white blood cell affected and the speed at which the disease progresses:

1. Acute Leukemias - These types of leukemia progress rapidly, with symptoms developing over a few weeks or months. They involve the rapid growth and accumulation of immature, nonfunctional white blood cells (blasts) in the bone marrow and peripheral blood. The two main categories are:
- Acute Lymphoblastic Leukemia (ALL) - Originates from lymphoid progenitor cells, primarily affecting children but can also occur in adults.
- Acute Myeloid Leukemia (AML) - Develops from myeloid progenitor cells and is more common in older adults.

2. Chronic Leukemias - These types of leukemia progress slowly, with symptoms developing over a period of months to years. They involve the production of relatively mature, but still abnormal, white blood cells that can accumulate in large numbers in the bone marrow and peripheral blood. The two main categories are:
- Chronic Lymphocytic Leukemia (CLL) - Affects B-lymphocytes and is more common in older adults.
- Chronic Myeloid Leukemia (CML) - Originates from myeloid progenitor cells, characterized by the presence of a specific genetic abnormality called the Philadelphia chromosome. It can occur at any age but is more common in middle-aged and older adults.

Treatment options for leukemia depend on the type, stage, and individual patient factors. Treatments may include chemotherapy, targeted therapy, immunotherapy, stem cell transplantation, or a combination of these approaches.

Retroviridae is a family of viruses that includes human immunodeficiency virus (HIV) and other viruses that primarily use RNA as their genetic material. The name "retrovirus" comes from the fact that these viruses reverse transcribe their RNA genome into DNA, which then becomes integrated into the host cell's genome. This is a unique characteristic of retroviruses, as most other viruses use DNA as their genetic material.

Retroviruses can cause a variety of diseases in animals and humans, including cancer, neurological disorders, and immunodeficiency syndromes like AIDS. They have a lipid membrane envelope that contains glycoprotein spikes, which allow them to attach to and enter host cells. Once inside the host cell, the viral RNA is reverse transcribed into DNA by the enzyme reverse transcriptase, which is then integrated into the host genome by the enzyme integrase.

Retroviruses can remain dormant in the host genome for extended periods of time, and may be reactivated under certain conditions to produce new viral particles. This ability to integrate into the host genome has also made retroviruses useful tools in molecular biology, where they are used as vectors for gene therapy and other genetic manipulations.

A cell line is a culture of cells that are grown in a laboratory for use in research. These cells are usually taken from a single cell or group of cells, and they are able to divide and grow continuously in the lab. Cell lines can come from many different sources, including animals, plants, and humans. They are often used in scientific research to study cellular processes, disease mechanisms, and to test new drugs or treatments. Some common types of human cell lines include HeLa cells (which come from a cancer patient named Henrietta Lacks), HEK293 cells (which come from embryonic kidney cells), and HUVEC cells (which come from umbilical vein endothelial cells). It is important to note that cell lines are not the same as primary cells, which are cells that are taken directly from a living organism and have not been grown in the lab.

Virus replication is the process by which a virus produces copies or reproduces itself inside a host cell. This involves several steps:

1. Attachment: The virus attaches to a specific receptor on the surface of the host cell.
2. Penetration: The viral genetic material enters the host cell, either by invagination of the cell membrane or endocytosis.
3. Uncoating: The viral genetic material is released from its protective coat (capsid) inside the host cell.
4. Replication: The viral genetic material uses the host cell's machinery to produce new viral components, such as proteins and nucleic acids.
5. Assembly: The newly synthesized viral components are assembled into new virus particles.
6. Release: The newly formed viruses are released from the host cell, often through lysis (breaking) of the cell membrane or by budding off the cell membrane.

The specific mechanisms and details of virus replication can vary depending on the type of virus. Some viruses, such as DNA viruses, use the host cell's DNA polymerase to replicate their genetic material, while others, such as RNA viruses, use their own RNA-dependent RNA polymerase or reverse transcriptase enzymes. Understanding the process of virus replication is important for developing antiviral therapies and vaccines.

Mink cell focus-inducing viruses (MCFs) are a group of gammaherpesviruses that have been isolated from minks and other animals. They are closely related to the human herpesvirus 4 (Epstein-Barr virus, or EBV), which is associated with various human malignancies such as Burkitt's lymphoma, nasopharyngeal carcinoma, and some types of lymphomas.

MCF viruses are characterized by their ability to induce the formation of foci of transformed cells in cultures of mink lymphocytes. These viruses have a complex structure, consisting of a double-stranded DNA genome enclosed within an icosahedral capsid and a lipid bilayer envelope.

MCF viruses are highly species-specific and do not infect human cells. However, they are closely related to the human gammaherpesviruses, and studies of MCF viruses have contributed significantly to our understanding of the molecular mechanisms underlying herpesvirus-induced cell transformation and oncogenesis.

It's worth noting that there is some controversy in the scientific community regarding the classification and nomenclature of these viruses, and different research groups may use slightly different definitions or names for similar viruses.

Viral DNA refers to the genetic material present in viruses that consist of DNA as their core component. Deoxyribonucleic acid (DNA) is one of the two types of nucleic acids that are responsible for storing and transmitting genetic information in living organisms. Viruses are infectious agents much smaller than bacteria that can only replicate inside the cells of other organisms, called hosts.

Viral DNA can be double-stranded (dsDNA) or single-stranded (ssDNA), depending on the type of virus. Double-stranded DNA viruses have a genome made up of two complementary strands of DNA, while single-stranded DNA viruses contain only one strand of DNA.

Examples of dsDNA viruses include Adenoviruses, Herpesviruses, and Poxviruses, while ssDNA viruses include Parvoviruses and Circoviruses. Viral DNA plays a crucial role in the replication cycle of the virus, encoding for various proteins necessary for its multiplication and survival within the host cell.

Viral genes refer to the genetic material present in viruses that contains the information necessary for their replication and the production of viral proteins. In DNA viruses, the genetic material is composed of double-stranded or single-stranded DNA, while in RNA viruses, it is composed of single-stranded or double-stranded RNA.

Viral genes can be classified into three categories: early, late, and structural. Early genes encode proteins involved in the replication of the viral genome, modulation of host cell processes, and regulation of viral gene expression. Late genes encode structural proteins that make up the viral capsid or envelope. Some viruses also have structural genes that are expressed throughout their replication cycle.

Understanding the genetic makeup of viruses is crucial for developing antiviral therapies and vaccines. By targeting specific viral genes, researchers can develop drugs that inhibit viral replication and reduce the severity of viral infections. Additionally, knowledge of viral gene sequences can inform the development of vaccines that stimulate an immune response to specific viral proteins.

RNA-directed DNA polymerase is a type of enzyme that can synthesize DNA using an RNA molecule as a template. This process is called reverse transcription, and it is the mechanism by which retroviruses, such as HIV, replicate their genetic material. The enzyme responsible for this reaction in retroviruses is called reverse transcriptase.

Reverse transcriptase is an important target for antiretroviral therapy used to treat HIV infection and AIDS. In addition to its role in viral replication, RNA-directed DNA polymerase also has applications in molecular biology research, such as in the production of complementary DNA (cDNA) copies of RNA molecules for use in downstream applications like cloning and sequencing.

Virus receptors are specific molecules (commonly proteins) on the surface of host cells that viruses bind to in order to enter and infect those cells. This interaction between the virus and its receptor is a critical step in the infection process. Different types of viruses have different receptor requirements, and identifying these receptors can provide important insights into the biology of the virus and potential targets for antiviral therapies.

Molecular sequence data refers to the specific arrangement of molecules, most commonly nucleotides in DNA or RNA, or amino acids in proteins, that make up a biological macromolecule. This data is generated through laboratory techniques such as sequencing, and provides information about the exact order of the constituent molecules. This data is crucial in various fields of biology, including genetics, evolution, and molecular biology, allowing for comparisons between different organisms, identification of genetic variations, and studies of gene function and regulation.

A provirus is a form of the genetic material of a retrovirus that is integrated into the DNA of the host cell it has infected. Once integrated, the provirus is replicated along with the host's own DNA every time the cell divides, and it becomes a permanent part of the host's genome.

The process of integration involves the reverse transcription of the retroviral RNA genome into DNA by the enzyme reverse transcriptase, followed by the integration of the resulting double-stranded proviral DNA into the host chromosome by the enzyme integrase.

Proviruses can remain dormant and inactive for long periods of time, or they can become active and produce new viral particles that can infect other cells. In some cases, proviruses can also disrupt the normal functioning of host genes, leading to various diseases such as cancer.

"Gene products, GAG" refer to the proteins that are produced by the GAG (Group-specific Antigen) gene found in retroviruses, such as HIV (Human Immunodeficiency Virus). These proteins play a crucial role in the structure and function of the viral particle or virion.

The GAG gene encodes for a polyprotein that is cleaved by a protease into several individual proteins, including matrix (MA), capsid (CA), and nucleocapsid (NC) proteins. These proteins are involved in the formation of the viral core, which encloses the viral RNA genome and associated enzymes required for replication.

The MA protein is responsible for binding to the host cell membrane during viral entry, while the CA protein forms the capsid shell that surrounds the viral RNA and NC protein. The NC protein binds to the viral RNA and helps to package it into the virion during assembly. Overall, GAG gene products are essential for the life cycle of retroviruses and are important targets for antiretroviral therapy in HIV-infected individuals.

A tumor virus infection is a condition in which a person's cells become cancerous or transformed due to the integration and disruption of normal cellular functions by a viral pathogen. These viruses are also known as oncoviruses, and they can cause tumors or cancer by altering the host cell's genetic material, promoting uncontrolled cell growth and division, evading immune surveillance, and inhibiting apoptosis (programmed cell death).

Examples of tumor viruses include:

1. DNA tumor viruses: These are double-stranded DNA viruses that can cause cancer in humans. Examples include human papillomavirus (HPV), hepatitis B virus (HBV), and Merkel cell polyomavirus (MCV).
2. RNA tumor viruses: Also known as retroviruses, these single-stranded RNA viruses can cause cancer in humans. Examples include human T-cell leukemia virus type 1 (HTLV-1) and human immunodeficiency virus (HIV).

Tumor virus infections are responsible for approximately 15-20% of all cancer cases worldwide, making them a significant public health concern. Prevention strategies, such as vaccination against HPV and HBV, have been shown to reduce the incidence of associated cancers.

A gammaretrovirus is a type of retrovirus, which is a virus that contains RNA as its genetic material and uses the reverse transcriptase enzyme to produce DNA from its RNA genome. Gammaretroviruses are enveloped viruses, meaning they have a lipid membrane derived from the host cell. They are also classified as simple retroviruses because their genome only contains the genes gag, pol, and env.

Gammaretroviruses are known to cause diseases in animals, including leukemias and immunodeficiencies. One example of a gammaretrovirus is the feline leukemia virus (FeLV), which can cause a variety of symptoms in cats, including anemia, lymphoma, and immune suppression.

Gammaretroviruses have also been implicated in some human diseases, although they are not thought to be major causes of human disease. For example, the human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus that is closely related to gammaretroviruses and can cause adult T-cell leukemia/lymphoma and tropical spastic paraparesis/ HTLV-associated myelopathy (TSP/HAM).

It's important to note that the classification of retroviruses has evolved over time, and some viruses that were once classified as gammaretroviruses are now considered to be part of other retrovirus genera.

A base sequence in the context of molecular biology refers to the specific order of nucleotides in a DNA or RNA molecule. In DNA, these nucleotides are adenine (A), guanine (G), cytosine (C), and thymine (T). In RNA, uracil (U) takes the place of thymine. The base sequence contains genetic information that is transcribed into RNA and ultimately translated into proteins. It is the exact order of these bases that determines the genetic code and thus the function of the DNA or RNA molecule.

Acute myeloid leukemia (AML) is a type of cancer that originates in the bone marrow, the soft inner part of certain bones where new blood cells are made. In AML, the immature cells, called blasts, in the bone marrow fail to mature into normal blood cells. Instead, these blasts accumulate and interfere with the production of normal blood cells, leading to a shortage of red blood cells (anemia), platelets (thrombocytopenia), and normal white blood cells (leukopenia).

AML is called "acute" because it can progress quickly and become severe within days or weeks without treatment. It is a type of myeloid leukemia, which means that it affects the myeloid cells in the bone marrow. Myeloid cells are a type of white blood cell that includes monocytes and granulocytes, which help fight infection and defend the body against foreign invaders.

In AML, the blasts can build up in the bone marrow and spread to other parts of the body, including the blood, lymph nodes, liver, spleen, and brain. This can cause a variety of symptoms, such as fatigue, fever, frequent infections, easy bruising or bleeding, and weight loss.

AML is typically treated with a combination of chemotherapy, radiation therapy, and/or stem cell transplantation. The specific treatment plan will depend on several factors, including the patient's age, overall health, and the type and stage of the leukemia.

Inbred strains of mice are defined as lines of mice that have been brother-sister mated for at least 20 consecutive generations. This results in a high degree of homozygosity, where the mice of an inbred strain are genetically identical to one another, with the exception of spontaneous mutations.

Inbred strains of mice are widely used in biomedical research due to their genetic uniformity and stability, which makes them useful for studying the genetic basis of various traits, diseases, and biological processes. They also provide a consistent and reproducible experimental system, as compared to outbred or genetically heterogeneous populations.

Some commonly used inbred strains of mice include C57BL/6J, BALB/cByJ, DBA/2J, and 129SvEv. Each strain has its own unique genetic background and phenotypic characteristics, which can influence the results of experiments. Therefore, it is important to choose the appropriate inbred strain for a given research question.

Virus integration, in the context of molecular biology and virology, refers to the insertion of viral genetic material into the host cell's genome. This process is most commonly associated with retroviruses, such as HIV (Human Immunodeficiency Virus), which have an enzyme called reverse transcriptase that converts their RNA genome into DNA. This DNA can then integrate into the host's chromosomal DNA, becoming a permanent part of the host's genetic material.

This integration is a crucial step in the retroviral life cycle, allowing the virus to persist within the host cell and evade detection by the immune system. It also means that the viral genome can be passed on to daughter cells when the host cell divides.

However, it's important to note that not all viruses integrate their genetic material into the host's genome. Some viruses, like influenza, exist as separate entities within the host cell and do not become part of the host's DNA.

Gibbon Ape Leukemia Virus (GaLV) is not exactly a "leukemia virus" in the sense that it directly causes leukemia in humans. Instead, GaLV is a type of retrovirus that primarily infects gibbons and some other non-human primates. It's important to note that GaLV is not known to infect or cause disease in healthy human beings.

GaLV has four subtypes (A, B, C, and D), with A and B being the most well-studied. These viruses have a close genetic relationship with certain human retroviruses, such as Human T-cell Leukemia Virus types I and II (HTLV-I/II). Although GaLV is not known to cause leukemia or any other diseases in humans directly, it has served as an important model for understanding the biology and pathogenesis of retroviruses, including those that can cause leukemia and other malignancies in humans.

The term "leukemia virus" is often used to describe retroviruses that can cause leukemia or lymphoma, such as HTLV-I/II and Human Immunodeficiency Virus (HIV). GaLV does not fit into this category for humans, but it's essential to understand its role in the context of retroviral research and comparative primatology.

Stoye JP, Moroni C, Coffin JM (March 1991). "Virological events leading to spontaneous AKR thymomas". Journal of Virology. 65 ( ... The Friend virus (FV) is a strain of murine leukemia virus. The Friend virus has been used for both immunotherapy and vaccines ... The murine leukemia viruses (MLVs or MuLVs) are retroviruses named for their ability to cause cancer in murine (mouse) hosts. ... The murine leukemia viruses are group/type VI retroviruses belonging to the gammaretroviral genus of the Retroviridae family. ...
Murine Leukemia Virus of AKR Origin". Journal of Virology. 47 (2): 317-328. doi:10.1128/JVI.47.2.317-328.1983. PMC 255263. PMID ... "Gibbon Ape Leukemia Virus Hall's Island: New Strain of Gibbon Ape Leukemia Virus". Journal of Virology. 29 (1): 395-400. doi: ... "Construction of Recombinant Retroviruses that Express the Human T Cell Leukemia Virus Type II and Human T Cell Leukemia Virus ... Coffin, JM; Hageman RC; Maxam AM; Haseltine WA (1978). "Structure of the Genome of Moloney Murine Leukemia Virus: A Terminally ...
over 1300 citations) Hartley, J. W.; Wolford, N. K.; Old, L. J.; Rowe, W. P. (1977). "A new class of murine leukemia virus ... "At least four viral genes contribute to the leukemogenicity of murine retrovirus MCF 247 in AKR mice". Journal of Virology. 53 ... over 800 citations) Lowy, D. R.; Rowe, W. P.; Teich, N.; Hartley, J. W. (1971). "Murine Leukemia Virus: High-Frequency ... over 700 citations) Staal, S. P.; Hartley, J. W.; Rowe, W. P. (1977). "Isolation of transforming murine leukemia viruses from ...
... leukemia virus, murine MeSH B04.820.650.375.525.020 - abelson murine leukemia virus MeSH B04.820.650.375.525.050 - akr murine ... leukemia virus, murine MeSH B04.909.574.807.375.525.020 - abelson murine leukemia virus MeSH B04.909.574.807.375.525.050 - akr ... leukemia virus, murine MeSH B04.909.777.731.375.525.020 - abelson murine leukemia virus MeSH B04.909.777.731.375.525.050 - akr ... leukemia virus MeSH B04.820.650.375.525.225 - friend murine leukemia virus MeSH B04.820.650.375.525.300 - gross virus MeSH ...
Staal SP, Hartley JW, Rowe WP (July 1977). "Isolation of transforming murine leukemia viruses from mice with a high incidence ... In 1977, a transforming retrovirus was isolated from the AKR mouse. This virus was named Akt-8, the "t" representing its ... "Entrez Gene: AKT1 v-akt murine thymoma viral oncogene homolog 1". Lindhurst MJ, Sapp JC, Teer JK, Johnston JJ, Finn EM, Peters ... AKT8 was isolated from a spontaneous thymoma cell line derived from AKR mice by cocultivation with an indicator mink cell line ...
... and the 1950s discoveries of Gross murine leukemia virus and polyoma virus". Studies in History and Philosophy of Science Part ... Leukemia in mice produced by a filterable agent present in AKR leukemic tissues with notes on a sarcoma produced by the same ... and the 1950s discoveries of Gross murine leukemia virus and polyoma virus". Studies in History and Philosophy of Biological ... So, since Gross believed that he discovered the polyoma virus first during his initial experiments with the leukemia virus, he ...
Reif AE, Allen JM (1964). "The AKR thymic antigen and its distribution in leukemias and nervous tissue". J. Exp. Med. 120 (3): ... the site of virus particle budding from cells, and Thy-1 is incorporated into virus particles as a result of this process.[ ... It is probably the most abundant glycoprotein of murine thymocytes, with about One million copies per cell covering up to 10-20 ... Thy-1.2 is expressed by most strains of mice, whereas Thy-1.1 is expressed by others such as AKR/J and PL mouse strains. The 25 ...
Staal SP, Hartley JW, Rowe WP (July 1977). "Isolation of transforming murine leukemia viruses from mice with a high incidence ... The "Ak" in Akt refers to the AKR mouse strain that develops spontaneous thymic lymphomas. The "t" stands for 'thymoma'; the ... the virus activates Akt1, which in turn causes the release of calcium. Treating the cells with Akt inhibitors before virus ... C. P. Rhoads by K. B. Rhoads at the Rockefeller Institute." When the oncogene encoded in this virus was discovered, it was ...
Stoye JP, Moroni C, Coffin JM (March 1991). "Virological events leading to spontaneous AKR thymomas". Journal of Virology. 65 ( ... The Friend virus (FV) is a strain of murine leukemia virus. The Friend virus has been used for both immunotherapy and vaccines ... The murine leukemia viruses (MLVs or MuLVs) are retroviruses named for their ability to cause cancer in murine (mouse) hosts. ... The murine leukemia viruses are group/type VI retroviruses belonging to the gammaretroviral genus of the Retroviridae family. ...
AKR *Murine leukemia virus*LDEV select virus isolates*E. cuniculi*Resistent to mousepox*Glomerular hylinosis*Thymic lymphoma* ... K virus lethal to suckling mice*MCMV*MMTV*Resistent to TMEV*Resistent to Salmonella enteritidis*Mast cells in spleen*Mammary ... Sendai virus *MHV*Salmonella typhimurium*Salmonella enteritidis*Helicobacter hepaticus: Typhlocolitis*- Resistant to ... K virus*Resistant to amyloidosis*Resistent to MHV*Skeletal muscle mineralization*Hepatacellular carcinoma with mets ...
AKR (endogenous) murine leukemia virus. *Friend murine leukemia virus. *MLV (Murine leukemia virus) ... Murine leukemia virus. Taxonomic Hierarchy , Viruses and Viroids , Riboviria , Pararnavirae , Artverviricota , Revtraviricetes ... Taxonomic Hierarchy , Viruses and Viroids , DNA and RNA reverse transcribing viruses , Ortervirales , Retroviridae , ... Abelson murine leukaemia virus. *Abelson murine leukemia virus. *AKR (endogenous) murine leukaemia virus ...
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B04 - VIRUSES. ABELSON LEUKEMIA VIRUS. ABELSON MURINE LEUKEMIA VIRUS. AKR VIRUS. AKR MURINE LEUKEMIA VIRUS. ... B04 - VIRUSES. ABELSON LEUKEMIA VIRUS. ABELSON MURINE LEUKEMIA VIRUS. AKR VIRUS. AKR MURINE LEUKEMIA VIRUS. ... GASTROENTERITIS VIRUS, MURINE. MURINE HEPATITIS VIRUS. GASTROENTERITIS VIRUS, PORCINE TRANSMISSIBLE. TRANSMISSIBLE ... GASTROENTERITIS VIRUS, MURINE. MURINE HEPATITIS VIRUS. GASTROENTERITIS VIRUS, PORCINE TRANSMISSIBLE. TRANSMISSIBLE ...
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Biochemistry, Metabolism:, Hereditary Factors:, Neoplasm:, Serology: Antigen,, Rickettsia, Virus:, Strains: AKR, BALB/C, C57BL/ ... Immunopathogenicity and oncogenicity of murine leukemia virus. Iii. Quantitation of spontaneous virus expression. ...
COMPARISON OF ENDOGENOUS MURINE LEUKEMIA-VIRUS PROVIRAL ORGANIZATION AND RNA EXPRESSION IN 3-METHYLCHOLANTHRENE-INDUCED AND ... Mice - Mice, Inbred AKR PubMed MeSh Term *Overview. Overview. subject area of * A polymorphism in the alpha 4 nicotinic ... SPONTANEOUS HYMIC LYMPHOMAS IN RF AND AKR MICE Journal Article * Interaction of the nicotinic cholinergic system with ethanol ...
Complexity and abundance of murine leukemia virus-related nuclear and messenger RNA sequences in mouse embryo cell lines which ... Growth arrest of AKR‐2B cells maintained in the presence of epidermal growth factor or 12‐O‐tetradecanolyhorbol‐13 acetate: ... Equivalent expression of endogenous murine leukemia virus-related genes in C3H/10T1/2 cells and chemically transformed ... Murine leukaemia C-type virus associated with functional murine carcinomas of endocrine origin. (1971). (12) ...
... contains DNA copies of an RNA tumor virus which is indistinguishable from the N-tropic murine leukemia virus of AKR mice [1]. ... The stem cell line, OTT6050AF1 BrdU, which is completely nonpermissive to productive infection by Moloney murine leukemia virus ... A murine teratocarcinoma stem cell line carries suppressed oncogenic virus genomes. Huebner, K., Tsuchida, N., Green, C., Croce ... The effect of lithium on murine hematopoiesis in a liquid culture system. Levitt, L.J., Quesenberry, P.J. N. Engl. J. Med. ( ...
Effective treatment of AKR leukemia with antibody to gp7 1 eliminates the neonatal burst of ecotropic AKR virus producing cells ... Effective treatment of AKR leukemia with antibody to gp7 1 eliminates the neonatal burst of ecotropic AKR virus producing cells ... Effective treatment of AKR leukemia with antibody to gp7 1 eliminates the neonatal burst of ecotropic AKR virus producing cells ... Effective treatment of AKR leukemia with antibody to gp7 1 eliminates the neonatal burst of ecotropic AKR virus producing cells ...
AKR murine leukemia virus. A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) isolated from spontaneous leukemia in AKR ... Friend murine leukemia virus. A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) producing leukemia of the reticulum- ... Moloney murine leukemia virus. A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) arising during the propagation of S37 ... virusMoloney murine leukemia virusSendai virusCapsidYellow fever virusTobacco Mosaic VirusMyxoma virusCowpox virusVariola virus ...
Leukemia in mice produced by a filterable agent present in AKR leukemic tissues with notes on a sarcoma produced by the same ... Small DNA tumor viruses: large contributors to biomedical sciences. Virology. 2009;384:256-9 .DOIPubMedGoogle Scholar ... This is a photograph of Sarah Elizabeth Stewart, PhD, MD (1905-1976), whose discoveries involving the murine polyomavirus with ... Induction of tumors in rats by tissue-culture preparations of SE polyoma virus. J Natl Cancer Inst. 1959;22:161-71 .PubMed ...
Abelson murine leukemia virus [B04.613.807.375.525.020] * AKR murine leukemia virus [B04.613.807.375.525.050] ... Leukemia Viruses, Murine Mouse Leukemia Viruses Murine Leukemia Virus Murine Leukemia Viruses Registry Number. txid11786. NLM ... Leukemia Virus, Gibbon Ape [B04.820.650.375.510] * Leukemia Virus, Murine [B04.820.650.375.525] * Abelson murine leukemia virus ... 2002; see LEUKEMIA VIRUSES, MURINE 1994-2001, see MOUSE LEUKEMIA VIRUSES 1966-1993; for GRAFFI VIRUS see GRAFFI VIRUS 1991, see ...
AKR/J. Leukocyte leukemia. *Friend leukemia virus - "conventional" (CFV). Leukocyte. 30 - 52.5 ... Effect of host strain and H-2 type on spontaneous regression of murine leukemia.. ... AKR/J. Leukocyte leukemia. *Friend leukemia virus - "regressing" (RFV). Leukocyte. 24 - 40 ...
Murine leukemia viruses (MuLV), L. Gross. * 1952. Curtain Call and Project Mouse published. ... This virus and experiments designed by Dr. Sundberg provide the proof of concept for the recombinant human cervical cancer ... Rudolf Jaenisch, now at the Massachusetts Institute of Technology (MIT), uses a virus to transfer DNA to mouse embryos, the ... The Nobel Prize in Physiology or Medicine 2008: Harald zur Hausen, "for his discovery of human papilloma viruses causing ...
c MLL-AF9 leukemia cells were co-cultured with or without NK cells. Frequency of Annexin-V + cells in MLL-AF9 leukemia cells ... Several commonly used laboratory mouse strains such as BALB/c, SJL, AKR, CBA, C3H and A do not express the NK1.1 antigen. For ... 16-5941 was used in Flow cytometry/Cell sorting to identify PI3Kγ as a novel key host protective factor in influenza virus ... 16-5941 was used in Flow cytometry/Cell sorting to investigate the influence of IL-15 on murine NK cell division and death ...
Ware, L.M.; Axelrad, A.A. 1972: Inherited resistance to N- and B-tropic murine leukemia viruses in vitro: evidence that ... Gresser, I.; Coppey, J.; Bourali, C. 1968: Inhibiting action of crude interferon on lymphoid leukemia in AKR mice. Comptes ... DeLong, D.C.; Baker, L.A.; Dillard, R.D.; Easton, N.R. 1967: Inhibition and regression of Friend leukemia virus-induced ... Knyszynski, A.; Gottlieb, P.; Fridkin, M. 1983: Inhibition by tuftsin of Rauscher virus leukemia development in mice. Journal ...
Certain viruses including oncolytic viruses such as the herpes simplex virus (HSV) and non-oncolytic viruses such as the ... We develop murine and humanized CAR constructs expressed in T cells from healthy donors and CLL patients that eradicate IGLV3- ... Mutation-specific CAR T cells as precision therapy for IGLV3-21R110 expressing high-risk chronic lymphocytic leukemia. ... Camundongos Endogâmicos AKR , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C3H , Camundongos Endogâmicos C57BL , ...
  • Different strains of mice may have different numbers of endogenous retroviruses, and new viruses may arise as the result of recombination of endogenous sequences. (wikipedia.org)
  • So in 1956, when Stewart approached Eddy for assistance growing the agent causing parotid tumors in mice, Eddy readily agreed and the 2 women rapidly worked out the characteristics of the agent that was not referred to as a virus in their publications until 1959. (cdc.gov)
  • Species of GAMMARETROVIRUS , containing many well-defined strains, producing leukemia in mice. (nih.gov)
  • MLVs include both exogenous and endogenous viruses. (wikipedia.org)
  • citation needed] The MLVs include both exogenous and endogenous viruses. (wikipedia.org)
  • The genomes of exogenous and endogenous murine leukemia viruses have been fully sequenced. (wikipedia.org)
  • Several commonly used laboratory mouse strains such as BALB/c, SJL, AKR, CBA, C3H and A do not express the NK1.1 antigen. (thermofisher.com)
  • Quantitation of spontaneous virus expression. (jax.org)
  • Effect of host strain and H-2 type on spontaneous regression of murine leukemia. (jax.org)
  • A highly immunogenic tumor transfected with a murine transforming growth factor type beta 1 cDNA escapes immune surveillance. (academicinfluence.com)
  • The mechanism by which latent viruses, such as genetically transmitted tumor viruses ( PROVIRUSES ) or PROPHAGES of lysogenic bacteria, are induced to replicate and then released as infectious viruses. (lookformedical.com)
  • The Friend virus (FV) is a strain of murine leukemia virus. (wikipedia.org)
  • Here, we use a BCR light chain neoepitope defined by a characteristic point mutation (IGLV3-21R110) for selective targeting of a poor-risk subset of chronic lymphocytic leukemia (CLL) with chimeric antigen receptor (CAR) T cells. (bvsalud.org)
  • Its deletion from the MCF13 virus dramatically reduced the incidence of thymic lymphoma and increased the latency of disease in comparison with the wild-type virus. (archive.org)
  • As Type C retroviruses, replicating murine leukemia viruses produce a virion containing a spherical nucleocapsid (the viral genome in complex with viral proteins) surrounded by a lipid bilayer derived from the host cell membrane. (wikipedia.org)
  • We have identified nucleotide sequences that regulate transcription in both a cell-type-specific and general manner in the long terminal repeat of the MCF13 murine leukemia virus. (archive.org)
  • The ability of a pathogenic virus to lie dormant within a cell (latent infection). (lookformedical.com)
  • The murine leukemia viruses are group/type VI retroviruses belonging to the gammaretroviral genus of the Retroviridae family. (wikipedia.org)
  • The type species of ORTHOPOXVIRUS, related to COWPOX VIRUS , but whose true origin is unknown. (lookformedical.com)
  • This is a photograph of Sarah Elizabeth Stewart, PhD, MD (1905-1976), whose discoveries involving the murine polyomavirus with Bernice Eddy, PhD, propelled the then-reluctant field of oncology to pursue viral etiologies of cancer. (cdc.gov)
  • At Eddy's suggestion, the virus was dubbed polyoma, which means many tumors, and they named it the SE (Stewart-Eddy) polyomavirus. (cdc.gov)
  • It took many decades before the seminal contributions of several virologists studying cancers were appreciated, such as Peyton Rous' 1911 discovery of the Rous sarcoma virus (which caused tumors in chickens), and discoveries of Richard Shope (rabbit fibroma) and John Bittner (mouse mammary carcinoma) in the 1930s. (cdc.gov)
  • This cleavage is essential for the Env incorporation into virus particles. (wikipedia.org)
  • The encoded proteins are trafficked to the plasma membrane, where they assemble into progeny virus particles. (wikipedia.org)
  • The expelling of virus particles from the body. (lookformedical.com)
  • The murine leukemia viruses (MLVs or MuLVs) are retroviruses named for their ability to cause cancer in murine (mouse) hosts. (wikipedia.org)
  • Among the latter MLVs are amphotropic viruses (Gr. amphos, "both") that can infect both mouse cells and cells of other animal species. (wikipedia.org)
  • Together they showed that the virus produced 20 types of mouse tumors and could cause tumors in other small mammals. (cdc.gov)
  • Any of the processes by which cytoplasmic factors influence the differential control of gene action in viruses. (lookformedical.com)
  • In 1944, when Stewart requested support to study the link between animal tumors and viruses, the directors of the NIH Laboratory of Microbiology and the National Cancer Institute (NCI) refused on the grounds that the proposal seemed dubious and that she lacked appropriate qualifications. (cdc.gov)
  • Stewart became medical director of the NCI Laboratory of Oncology and spent the remainder of her life researching several oncogenic viruses (e.g. (cdc.gov)
  • Effective treatment of AKR leukemia with antibody to gp7 1 eliminates the neonatal burst of ecotropic AKR virus producing cells. (duke.edu)
  • Process of growing viruses in live animals, plants, or cultured cells. (lookformedical.com)
  • A newly identified protein-binding site (MLPal) located within DEN affects transcription only in T cells, and its deletion attenuates the ability of an MCF13 virus with a single enhancer repeat to induce thymic lymphoma. (archive.org)
  • We develop murine and humanized CAR constructs expressed in T cells from healthy donors and CLL patients that eradicate IGLV3-21R110 expressing cell lines and primary CLL cells, but neither cells expressing the non-pathogenic IGLV3-21G110 light chain nor polyclonal healthy B cells. (bvsalud.org)
  • To understand Stewart's role in catalyzing viral oncology research, it is necessary to recognize that until the 1950s, scientists dismissed the idea that viruses could cause cancer. (cdc.gov)
  • The results of their collaboration were picked up by a 1959 Time Magazine cover story, citing John Heller, then the NCI director, "the hottest thing in cancer research is research on viruses as possible causes of cancer. (cdc.gov)
  • Virus shedding is an important means of vertical transmission (INFECTIOUS DISEASE TRANSMISSION, VERTICAL). (lookformedical.com)
  • They also demonstrated that the virus causes cell necrosis and proliferation in cell culture, that it is highly antigenic, and that it leads to formation of specific antibodies in infected animals whether or not tumors develop. (cdc.gov)
  • B virus (HBV), hepatitis C virus (HCV), or human immunodeficiency virus (HIV). (cdc.gov)
  • In 1954, Eddy had been sidelined for whistleblowing about the presence of live virus in Jonas Salk's inactivated polio vaccine (the infamous Cutter incident). (cdc.gov)
  • Specific molecular components of the cell capable of recognizing and interacting with a virus, and which, after binding it, are capable of generating some signal that initiates the chain of events leading to the biological response. (lookformedical.com)