Immunodiffusion: detection of a murine leukemia virus (Rauscher)

Homologous and heterologous antiserums from several species of animals have been prepared against the Rauscher murine leukemia virus. The Ouchterlony technique, adapted to very small quantities, has been used to demonstrate at least two or three antigens in Rauscher virus preparations. Both infected-host materials and tissue-culture fluids were used as antigens. When monkey antiserum was used, one of the Rauscher virus antigens cross-reacted with an antigen in the virus strains isolated by Friend and Moloney, but there was apparently no reaction with the Moloney virus when guinea-pig antiserum was used.     

Leukemogenic activity of filtrates from radiation-induced lymphoid tumors of mice

Cell-free filtrates of x-ray-induced lymphoid tumors of strain C57BL/ Ka mice have elicited, on injection into newborn isologous hosts, a lymphoma incidence of 15 to 19 percent. In control mice of the same subline, the incidence of spontaneous lymphoma is about 1 percent. No leukemogenic activity could be detected in filtrates from thymi harvested at 2 to 32 days following completion of x-ray treatment. Activity was evident at 64 days and was perhaps somewhat greater at 128 days. Serial cell-free passage of filtrates in newborn F(1) hybrid mice resulted in a marked increase in lymphoma incidence (69 percent), coupled with a shortening of the median latency. Supplementary x-irradiation failed to enhance the activity of filtrates after neonatal injection.     

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.     

Resistance of mice infected with Moloney leukemia virus to Friend virus infection

Mice inoculated with the Moloney strain of mouse lymphoid-leukemia virus showed marked diminution of spleen weight response to infection with Friend leukemia virus given 3 to 4 weeks later.     

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.     

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.     

整合猪瘟病毒囊膜蛋白的假型鼠白血病病毒感染性的研究

通过反转录-聚合酶链式反应(RT-PCR)扩增了猪瘟病毒(CSFV)的E0、E2和E012基因并进行了克隆与鉴定。构建了真核表达载体pcDNA-E0、pcDNA-E2和pcDNA-E012,通过与鼠白血病病毒(MuLV)假型病毒构建体系的两种质粒pHIT60和pHIT111瞬时共转染人胚肾细胞(293T),48h后收集假型病毒上清液,将假型病毒上清液超速离心后用抗CSFV的多抗进行Western-blot检测。结果证明E012蛋白能够在假型病毒颗粒表面表达,说明E012能够整合到此病毒粒子表面;用其感染多种宿主细胞,48h后检测发现在猪肾细胞(SK6,PK15)和猪睾丸细胞(ST)上,标记基因LacZ能有效表达,证实构建的CSFV假型病毒具有感染性。     

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.     

Susceptibility to two strains of Friend leukemia virus in mice

A mutant strain of the Friend leukemia virus is described. The parental virus strain, passaged through ICR/Ha mice, shows no or very little activity by the spleen-focus assay in BALB/c mice (by comparison with highly susceptible DBA/2 and ICR/Ha mice) and produces typical Friend disease in these mice only exceptionally; susceptibility to this strain of virus is recessive in the (C57BL/6 x DBA/2) F(1). By contrast, the mutant virus strain is as active in BALB/c mice as in DBA/2 or ICR/Ha mice; susceptibility to the mutant virus strain is dominant in the (C57BL/6 x DBA/2) F(1).     

Genetic polymorphism of the bovine leukemia virus in the Russian federation

Nucleotide sequence of a section of the Env 105 gene of bovine leukemia provirus isolates, obtained from farm animals in different regions of Russia, was determined. Conducted phylogenetic analysis has allowed us to assess heterogeneity of the studied population of the bovine leukemia virus (BLV). Based on results of BLV genetic diversity, four virus’s genotypes—I, II, IV, and VII with dominating genotype IV—were detected.     

Human T-cell leukemia virus (HTLV-I) antibodies in Africa

Antibodies specific for human T-cell leukemia-lymphoma virus type I (HTLV-I) were demonstrated in serum samples from various groups of people in South Africa, Uganda, Ghana, Nigeria, Tunisia, and Egypt. The samples had been collected for other purposes and were presumably selected without bias toward clinical conditions associated with HTLV infections. Regional differences in antibody positivity were observed, indicating widely distributed loci of occurrence of HTLV on the African continent in people of both black and white ancestry. Two patients with high titers of antibody to HTLV-I had some signs of adult T-cell leukemia-lymphoma. In several groups a high frequency of false positive serum reactions was indicated when specific confirmation steps were included in the assay. Further characterization of these sera revealed highly elevated immunoglobulin levels, possibly due to polyclonal activation of immunoglobulin synthesis in these subjects. The possibility that related cross-reactive human retroviruses coexist in the same groups was not eliminated.     

Activation of spontaneous murine leukemia virus-related antigen by lymphocytic choriomeningitis virus

Persistent infection with lymphocytic choriomeningitis (LCM) virus activates a phenotypic expression of murine leukemia viruis-related antigen. NZB and (NZB x NZW)F(1) mice, which normally carry large amounts of Gross virus, and C57BL/6 and NZW mice, which normally carry little virus, were infected with LCM virus. All had Gross soluble antigen in their plasmas at 3 months of age, while noninfected matched controls of all strains did not. This effect was seen after infection with LCM virus that was tissue passed or plaque purified. Similarly, cultures of mouse-embryo fibroblasts produced Gross soluble antigen when infected with LCM virus, but noninfected cultures failed to do so.     

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.     

Isolation and transmission of human retrovirus (human t-cell leukemia virus)

Nine new isolates of human T-cell leukemia-lymphoma virus (HTLV) were obtained from cells of seven patients with malignancies of mature T cells and from two clinically normal relatives of a T-cell leukemia patient. These people were from the United States, Israel, the West Indies, and Japan. The virus was detected in the fresh T cells and was isolated from the established T-cell lines. Each isolate is closely related to the first HTLV isolate, and all the new HTLV isolates were transmitted into normal human T cells obtained from the umbilical cord blood of newborns.     

Identification of a cellular cofactor required for infection by feline leukemia virus

Retroviral infection involves continued genetic variation, leading to phenotypic and immunological selection for more fit virus variants in the host. For retroviruses that cause immunodeficiency, pathogenesis is linked to the emergence of T cell-tropic, cytopathic viruses. Here we show that an immunodeficiency-inducing, T cell-tropic feline leukemia virus (FeLV) has evolved such that it cannot infect cells unless both a classic multiple membrane-spanning receptor molecule (Pit1) and a second coreceptor or entry factor are present. This second receptor component, which we call FeLIX, was identified as an endogenously expressed protein that is similar to a portion of the FeLV envelope protein. This cellular protein can function either as a transmembrane protein or as a soluble component to facilitate infection.     

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.