Demonstration of biological activity of a murine leukemia virus of New Zealand black mice

Although New Zealand Black mouse embryo and adult tissues show evidence of murine leukemia viral particles and antigens, efforts to demonstrate biological activity of a murine leukemia virus by standard methods have proved negative. Cocultivation of tissues of these mice with non-virus-yielding hamster cells transformed by Moloney sarcoma virus, however, has resulted in the rescue of a pseudotype sarcoma virus, presumably carrying the New Zealand Black mouse leukemia virus coat. This virus has an unusual host restriction, producing foci of cell alteration only in rat cells.     

Viral infection across species barriers: reversible alteration of murine sarcoma virus for growth in cat cells

Infection of cat embryo cells by a centrifugally induced aggregate of murine sarcoma virus and feline leukemia virus gave rise to a defective, focus-forming virus which propagated in cat cells, but not in mouse cells. This virus, apparently enveloped with a feline leukemia virus coat, was later subjected to aggregation with murine leukemia virus, whereupon it regained the capacity for growth in mouse cells.     

Titration patterns of a murine sarcoma-leukemia virus complex: evidence for existence of competent sarcoma virions

Stocks of inurine sarcoma virus show titration patterns ranging from one-to two-hit kinetics. The comparison of various titrations of this virus, both with and without added helper virus, to theoretical model systems composed of defined constituents, suggests the existence of a sarcoma virus that does not need coinfectinig murine leukemia virus to be manifested as a focus-forming unit. The behavior of such nondefective particles is compatible with a postulated leukemia-sarcoma virus hybrid.     

Radiation leukemia virus: quantitative tissue culture assay

Radiation leukemia virus does not propagate in tissue cultures from either Swiss or C57BL mouse embryos, but it does augment focus formation by the defective Moloney leukemia pseudotype of murine sarcoma virus in Swiss mouse cells and thus can be quantitatively assayed.     

Xenotropic viruses: murine leukemia viruses associated with NIH Swiss, NZB, and other mouse strains

Murine leukemia virus activity is present in tissues from NIH Swiss and other mouse strains after cocultivation with nonvirus-yielding rat cells transformed by Harvey sarcoma virus. The resulting pseudotype sarcoma virus has the same type-specific coat as the virus previously isolated from New Zealand black (NZB) mice, and, like the NZB virus, it is unable to infect mouse cells. The results show that this NZB type virus is endogenous in other strains of mice and is xenotropic; that is, it grows only in cells foreign to the host. This is the first clear demonstration that NIH Swiss mice also carry indigenous infectious murine leukemia virus.     

Complete nucleotide sequence and organization of the Moloney murine sarcoma virus genome

The complete nucleotide sequence of a mammalian transforming retrovirus. Moloney murine sarcoma virus, has been determined. MSV, recombinant virus derived of helper viral and cellular sequences, possesses termini resembling prokaryotic transposable elements. The viral genome has the coding capacity for the Moloney murine leukemia virus gag gene product and contains large deletions in pol and env genes. A large open reading frame encompassing its cell-derived sequences codes for its putative transforming protein. The nature of some of the important domains in the viral genome has been established, and their structure is discussed in relation to their function.     

Transformation of chick embryo neuroretinal cells by Rous sarcoma virus in vitro: induction of cell proliferation

Neuroretinal cells from 7-day-old chick embryos are transformed and induced to proliferate after infection with Rous sarcoma virus in vitro. Susceptibility of neuroretinal cells to the virus is also dependent on the stage of development since infection of cells from 10-day-old embryos is uneffective.     

Glycopeptides from the surface of control and virus-transformed cells

Glycopeptides were removed by trypsin digestion from the surface of control cells and cells transformed by Rous sarcoma virus, murine sarcoma virus, or polyoma virus. After digestion with pronase, the glycopeptides were analyzed by gel filtration. The elution profiles suggest that there are differences in the glycopeptides from the surface of control cells and those from transformed cells.     

Murine leukemia virus: high-frequency activation in vitro by 5-iododeoxyuridine and 5-bromodeoxyuridine

Cells of embryos of the high leukemic mouse strain AKR can be grown in culture as virus-negative cell lines. However, these lines and clonal sublines uniformly have the capacity to initiate synthesis of murine leukemia virus. Exposure of the cells to 5-iododeoxyuridine or 5-bromodeoxyuridine induced synthesis of virus in as high as 0.1 to 0.5 percent of the cells; many of the cells were producing virus as soon as 3 days after initiation of treatment. Induction of virus by these drugs is several orders of magnitude greater than that obtained with any other treatment tested. These studies indicate that the full genome of murine leukemia virus is present in an unexpressed form in all AKR cells and provide a potentially powerful technique for activating leukemia virus genomes in other cell systems.     

DNA of Rous sarcoma virus: its nature and significance

Purified preparations of Rous sarcoma virus (an avian tumor virus with an RNA genome) contain small amounts of double-stranded DNA. This DNA cannot be hybridized to viral RNA, but will reanneal completely with the DNA of avian cells. Extensive substitution of bromodeoxyuridine for thymidine in "viral" DNA does not photosensitize the biological activity of the virus. These observations indicate that the DNA associated with Rous sarcoma virus is derived from the DNA of the avian host cell, and is probably devoid of any function in the life cycle of the virus.     

Nucleotide sequence of the p21 transforming protein of Harvey murine sarcoma virus

Harvey murine sarcoma virus is a retrovirus which transforms cells by means of a single virally encoded protein called p21 has. We have determined the nucleotide sequence of 1.0 kilobase in the 5' half of the viral genome which encompasses the has coding sequences and its associated regulatory signals. The nucleotide sequence has identified the amino acid sequence of two additional overlapping polypeptides which share their reading frames and the carboxyl termini with p21 but which contain additional NH2-terminal amino acids.     

Nucleotide sequence of the Rasheed rat sarcoma virus oncogene: new mutations

The nucleotide sequence of the oncogene of the Rasheed strain of rat sarcoma virus was determined. The oncogene (Ra-v-ras) encodes a 29,000-dalton (p29) transforming protein. This protein is distinct from the immunologically related 21,000-dalton protein (p21) of the Harvey murine sarcoma virus in its amino terminus and in having additional mutations in its carboxyl terminus. Although the functional significance of these changes is unknown, they appear to occur only in rat sarcoma virus.     

Viral RNA subunits in cells transformed by RNA tumor viruses

Single-stranded 35S and 20S viral RNA species are synthesized in virus-producing mouse and rat cells transformed by the murine sarcoma virus. A transformed hamster cell line that does not produce virus synthesizes 35S, but not 20S viral RNA.     

Nucleotide sequence of the oncogene encoding the p21 transforming protein of Kirsten murine sarcoma virus

The transforming protein ofKirsten murine sarcoma virus (Ki-MuSV) is a virally encoded 21-kilodalton protein called p21 kis. The sequences encoding p21 kis were genetically localized to a 1.3-kilobase segment near the 5' end of the viral genome by assaying the capacity of a series of defined deletion mutants of molecularly cloned Ki-MuSV DNA to induce focal transformation of mouse cells. Nucleotide sequencing of a portion of this region has led to the identification of an open reading frame of 567 nucleotides coding for p21 kis protein.     

Neoplastic transformation of human epidermal keratinocytes by AD12-SV40 and Kirsten sarcoma viruses

Recent investigations have begun to dissect the number and nature of genetic alterations associated with cancer cells. In the present study, primary human epidermal keratinocytes acquired indefinite life-span in culture but did not undergo malignant conversion in response to infection with a hybrid of adenovirus 12 and simian virus 40. Addition of Kirsten murine sarcoma virus, which contains a K-ras oncogene, to these cells induced morphological alterations associated with the acquisition of neoplastic properties. These findings demonstrate the malignant transformation of human primary epithelial cells in culture and support a multiple-step process for neoplastic conversion.     

Properties of a normal mouse cell DNA sequence (sarc) homologous to the src sequence of Moloney sarcoma virus

A 15.0-kilobase (kb) Eco RI DNA fragment from normal mouse Balb/c genomic DNA that contains sequences (sarc) homologous to the acquired cell sequences (src) of Moloney sarcoma virus (MSV) has been cloned in phage lambda. The sarc region (1.2 to 1.3 kb) of the 15.0-kb cell fragment is indistinguishable from the src region of two isolates of MSV as judged by heteroduplex and restriction endonuclease analyses. The cellular sequences flanking sarc show no homology to other MSV sequences. Whereas cloned subgenomic portions of MSV that contain src transformed NIH-3T3 cells in vitro, the cloned sarc fragment is inactive.     

Inhibition of chemical carcinogenesis by viral vaccines

The incidence of 3-methylcholanthrene-induced subcutaneous tumors was significantly reduced by a single injection of inactivated type C RNA viral vaccine. Rauscher leukemia virus vaccine reduced the incidence of sarcomas from 78 to 50 percent in the BALB/cCr mouse. Radiation leukemia virus vaccine and a vaccine from a wild murine leukemia virus derived from a 3-methylcholanthrene tumor reduced the incidence of sarcoma from 86 percent to 33 and 37 percents, respectively, in the C57BL/6 mouse. These reductions in tumor incidence by virus vaccines help support the concept that type C RNA viruses serve as determinants of chemically induced cancer; additional studies of vaccines made with more purified virus preparations are necessary.     

大眼鰤鲈鱼真皮肿瘤病毒（WDSV）辅助基因orfA和orfC多抗的制备及初步应用

【目的】制备大眼鰤鲈鱼真皮肿瘤病毒(WDSV)辅助基因orfA和orfC的多克隆抗体,并用其检测酵母和肿瘤细胞中目的蛋白的表达。【方法】以WDSV基因组序列为模板,PCR扩增WDSV orfA和orfC基因,分别构建其原核表达载体,转化Rosseta（DE3）感受态细胞,经IPTG诱导表达并纯化重组蛋白后,采用皮下多点注射结合耳静脉加强免疫的方法免疫新西兰白兔,制备抗orfA和抗orfC的多克隆抗体,用Western blot法检测抗体的特异性。用制备的多克隆抗体检测orfA和orfC融合蛋白在酵母和HeLa299、SPC-A-1肿瘤细胞中的表达。【结果】PCR扩增获得了WDSV orfA和orfC基因。成功构建了orfA和orfC基因的原核表达载体并进行了诱导表达,orfA和orfC重组融合蛋白以包涵体形式存在;采用皮下注射结合耳静脉加强免疫有效地提高了抗体效价,成功制备得到了兔抗orfA和兔抗orfC血清,抗体效价达1∶8 000～1∶10 000;通过Western blot法,利用上述抗血清分别检测到了原核表达的目的蛋白及酵母和肿瘤细胞中表达的目的蛋白。【结论】制备得到的抗orfA和抗orfC多克隆抗体具有很好的特异性,能够用于原核表达、酵母和肿瘤细胞中表达的目的蛋白的Western blot检测。     

Three distinct genes in human DNA related to the transforming genes of mammalian sarcoma retroviruses

Southern blot hybridization was used to identify human and other vertebrate DNA sequences that were homologous to cloned DNA fragments containing the oncogenic nucleic acid sequences of three different type C mammalian retroviruses (simian sarcoma virus, the Snyder-Theilen strain of feline sarcoma virus, and the Harvey strain of murine sarcoma virus). Each onc gene counterpart has a single genetic locus, which probably contains non-onc intervening sequences. The human DNA sequences may represent genes important to cell growth or cell differentiation, or both. Their identification and isolation may allow elucidation of their role in these processes and in neoplasias.     

Mouse leukemia virus activation by chemical carcinogens

The induction of lymphomas in C57BL mice by methylcholanthrene, urethan, or diethylnitrosamine was accompanied by the development of murine leukemia viral antigen in most of the lymphoid tumors. The cell-free transmission of lymphomas induced by methylcholanthrene and the development of antibody to murine leukemia virus prior to the detection of overt lymphoma in these mice suggest that unmasking of a latent leukemia virus is an indigenous actuating cause of the lymphomas.