Feline leukemia virus: occurrence of viral antigen in the tissues of cats with lymphosarcoma and other diseases

Felinie leutkemia viruts antigen is demonstrable by immunodiffusion with rabbit precipitating antiserum to purified felinie leukemia virus. The felinie leukemia virus antigen was found in the tissues of 25 of 33 cats with lymphosarcoma and of 5 of 13 cats with infectious peritonitis. Its presence was correlated with the occurrence of felinie leukemia virus demonstrable by electron microscopy. The one clinically normal cat giving a positive test for feline leukemia virus antigen belonged to a household in which two cats had developed lymphosarcoma. With the exception of a dog with lymphosarcoma induced by feline leukemia virus, the antigent was absent from lymphosarcoma and nonlymphomatous tumors of other species (man, dog, cow, goat, or pig).     

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.     

Reversion of murine sarcoma virus transformed mouse cells: variants without a rescuable sarcoma virus

Murine sarcoma virus transformed mouse 3T3 cells, which are negative for murine leukemia virus and which yield sarcoma virus after superinfection with murine leukenmia virus, spotaneously give rise to flat variants front which murine sarcoma virus can no longer be rescued. The revertants support leukemia viruis growth and show an enhanced sensitivity to murine sarcoma superinfection and, like normal cells, do not release RNA-dependent DNA polymerase activity. Because revertants could be obtained with high frequency from progeny of single transformed cells, each cell that containts the sarconma virus genome seems to have the capacity to suppress or eliminate an RNA tumor virus native to its species of origin.     

Segregation of loci for C-type virus induction in strains of mice with high and low incidence of leukemia

Multiple genetic loci for induction of murine leukemia viruses are demonstrated in cells of the high leukemic incidence C58 mouse strain. The biologic properties of viruses at C58 inducibility loci are clearly distinguishable from those of viruses activated from mouse cells containing a locus for virus induction of the low leukemia incidence BALB/c strain. These findings are consistent with the hypothesis that the genes for virus induction in normal mouse embryo cells represent viral structural information.     

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.     

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.     

Antibody to leukemia virus: widespread occurrence in inbred mice

Mice from a wide variety of inbred strains produce immunoglobulin G antibody against murine leukemia virus. This is contrary to the common view that the mouse is immunologically tolerant to its endogenous leukemia virus.     

Gene for T-cell growth factor: location on human chromosome 4q and feline chromosome B1

T-cell growth factor (TCGF) or interleukin-2 (IL-2), an immunoregulatory lymphokine, is produced by lectin- or antigen-activated mature T lymphocytes and in a constitutive manner by certain T-cell lymphoma cell lines. By means of a molecular clone of human TCGF and DNA extracted from a panel of somatic cell hybrids (rodent cells X normal human lymphocytes), the TCGF structural gene was identified on human chromosome 4. In situ hybridization of the TCGF clone to human chromosomes resulted in significant labeling of the midportion of the long arm of chromosome 4, indicating that the TCGF gene was located at band q26-28. Genomic DNA from a panel of hybrids prepared with HUT-102 B2 cells was examined with the same molecular clone. In this clone of cells, which produces human T-cell leukemia virus, the TCGF gene was also located on chromosome 4 and was apparently not rearranged. The homologous TCGF locus in the domestic cat was assigned to chromosome B1 by using a somatic cell hybrid panel that segregates cat chromosomes. Linkage studies as well as high-resolution G-trypsin banding indicate that this feline chromosome is partially homologous to human chromosome 4.     

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.     

Murine leukemia virus: restriction in fused permissive and nonpermissive cells

Cultures of human cells nonpermissive for mouse leukemia virus replication could not be induced to support virus replication by homologous fusion in the presence of Moloney leukemia virus. Human cells were also fused with permissive mouse cells, and the fate of the virus in heterokaryons was determined by a simultaneous autoradiography and fluorescent antibody technique. Heterokaryons containing the full chromosome complement of both cells were likewise nonpermissive for virus synthesis, but hybrids of human and mouse cells, which lacked up to half of the human chromosome complement, were permissive for virus synthesis. The results suggest that human cell genes can direct a repressive control over mouse leukemia virus replication.     

Virus particles and murine leukemia virus complement-fixing antigen in neoplastic and nonneoplastic cell lines

Twenty-seven lines of murine tissue cultures derived from 12 different cell pools and grown on various media were examined with the electron microscope for morphologically detectable virus particles. They were also tested for complement-fixing mouse leukemia virus antigens and for recoverable virus. A 100-percent correlation between results obtained by these two methods is reported.An additional 19 lines from 8 different cell pools were examined for either virus particles or complement-fixing antigens. All lines were assayed for neoplastic transformation. Seven cell pools gave rise to lines showing evidence of contamination with leukemia virus. Since most of these lines had also undergone "spontaneous" neoplastic transformation in vitro, this virus cannot be excluded as a possible cause of the neoplastic change, or of influencing it. The remaining cell pools gave rise to lines with no evidence of contamination with leukemia virus;but most of these lines also underwent similar transformation. These results suggest that "spontaneous" neoplastic transformation can occur in the absence of detectable mouse leukemia virus.     

Active genes are sensitive to deoxyribonuclease I during metaphase

The active exogenous murine leukemia virus sequences of mouse cells growing in culture are preferentially digested by deoxyribonuclease I in metaphase chromosomes. As determined by nuclear nick translation, all of the gene sequences of these cells active during interphase are in a deoxyribonuclease I-sensitive conformation during metaphase. This method of nick translation can therefore be used to label chromosomes in situ in order to visualize the active regions of the genome.     

Type C RNA tumor viruses as determinants of chemical carcinogenesis: effects of sequence of treatment

Fischer rat embryo cells were treated with 3-methylcholanthrene before or after inoculation with Rauscher murine leukemia virus. Transformation was not observed in untreated control cultures, cultures given virus or 3-methyl-cholanthrene alone, or cultures treated first with 3-methylcholanthrene followed by inoculation with the virus after removal of the chemical. Transformation was dependent upon the presence of Rauscher murine leukemia virus at the time of chemical treatment.     

Genetic mapping of the Fv-1 lcous of the mouse

The Fv-l locus of the mouse, a major determinant of the biology of murine leukemia virus, is very closely linked to Gpd-1 on chromosome 4 (linkage group VIII).     

Isolation of a T-lymphotropic virus from domestic cats with an immunodeficiency-like syndrome

A highly T-lymphotropic virus was isolated from cats in a cattery in which all the animals were seronegative for feline leukemia virus. A number of cats in one pen had died and several had an immunodeficiency-like syndrome. Only 1 of 18 normal cats in the cattery showed serologic evidence of infection with this new virus, whereas 10 of 25 cats with signs of ill health were seropositive for the virus. Tentatively designated feline T-lymphotropic lentivirus, this new feline retrovirus appears to be antigenically distinct from human immunodeficiency virus. There is no evidence for cat-to-human transmission of the agent. Kittens experimentally infected by way of blood or plasma from naturally infected animals developed generalized lymphadenopathy several weeks later, became transiently febrile and leukopenic, and continued to show a generalized lymphadenopathy 5 months after infection.     

Suppression of gamma interferon production by inactivated feline leukemia virus

Supernatants from cultures of normal feline lymphocytes stimulated with Staphylococcus enterotoxin A showed antiviral activity, characterized as a gamma-like interferon. With the addition of inactivated feline leukemia virus, markedly less interferon was produced. The reduction in interferon production was not attributable to lowered lymphocyte viability or reduced mitogenic properties of Staphylococcus enterotoxin A and appears to be a direct retroviral effect. This finding may reflect clinically relevant events that may contribute to the development of the feline or human states of acquired immunodeficiency.     

广州市部分区域猫泛白细胞减少症流行现状调查

[目的]了解猫泛白细胞减少症病毒在广州家猫和流浪猫中的流行情况,分析FPV威胁广州家猫和流浪猫的潜在风险。[方法]采用猫泛白细胞减少症免疫胶体金快速检测试纸条和PCR检测方法对广州5家动物医院采集的3 004份猫样品进行检测与分析。[结果]猫泛白细胞减少症免疫胶体金快速检测试纸条检出10份疑似猫泛白细胞减少症阳性样品,采用猫泛白细胞减少症PCR检测方法检出13份猫泛白细胞减少症阳性样品。13份阳性样品来源于96份具有临床症状且未免疫样品,49份家猫样品中有6份呈阳性,47份流浪猫样品中有7份呈阳性,阳性率分别为12.2%(6/49)和14.9%(7/47),发病季节以9~10月多发,发病年龄集中在0~6月龄。[结论]与外界接触和未免疫疫苗可能是导致猫感染FPV的重要原因。因此,家猫加强疫苗接种,减少与未知免疫背景的猫只接触,减少家猫感染FPV的潜在风险。