Transformation, in vitro, of cerebral hamster cells by polyoma virus]

A cell line called HCxPy was obtained in vitro by transformation of dissociated hamster brain cell cultures by polyoma virus. The first foci of transformed cells became evident 90 to 120 days after viral infection. This cell line is now at the 46th passage. The cells appear tumorigenic for hamsters after subcutaneous and intracerebral injection. They carry the polyoma virus T and cell surface antigens. Good evidence for astrocytic differentiation can be found by morphological examination of the tumours and of the cultured cells.     

Immunologic blood-brain barrier in the polyoma virus--Syrian hamster system]

The authors report premilinary results of an experiment on permeability of the blood-brain barrier (BBB) to anti-tumor virus-induced immunological factors in the polyoma virus/Syrian Hamster system. The animals were protected by subcutaneous or intracranial injections with virus before challenge with polyoma virus transformed cells by both routes. BBB seemed to be permeable to the efferent part of the subcutaneously induced immune reaction. On the contrary, antigenic information introduced in the central nervous system was trapped inside the BBB. Thus the BBB might offer a "one-way" permeability in this system.     

A thermosensitive inhibitor of the replication of polyomavirus, an extract from BHK2I cells transformed by the Tsa mutant of this virus

BHK21 cells transformed by wild type or Ts3 mutant polyoma virus contain an inhibitor of polyoma virus replication when grown at permissive (36 degrees C) as well as non-permissive temperature (39 +/- 0.5 degrees C). Cells transformed by the Tsa mutant contain the inhibitor at the permissive but not at the non-permissive temperature. The inhibitor reappears in the latter cells however, upon shift from the non-permissive to the permissive temperature. If a reversible protein inhibitor (methionyl-adenylate, reversible inhibitor of the aminoacyl-t-RNA synthetase) is applied during the temperature shift experiments, the inhibitor does not reappear indicating that new protein synthesis is required for the recovery of its activity.     

Correlation between agglutinability of concanavalin A and nucleic acid synthesis induced by polyoma virus]

We have previously shown the induction of agglutinability by concanavalin A by abortice infection of BHK 21 cells with polyoma virus. In this system, the maximal agglutination occurred simultaneously with the first mitosis. Using inhibitors of macromolecule synthesis in an amitotic system, we showed that this agglutinability was correlated with cell DNA synthesis.     

Different sensitivities to ultraviolet rays of various functions of the polyoma virus. Stimulation of the synthesis of cellular DNA]

Peritoneal Mouse macrophage were used to study the stimulation of cell DNA synthesis by polyoma virus. Using ultraviolet-irradiated polyoma virus, it was possible to show a difference between the inactivations of infectivity and of induction of DNA synthesis. By statistically analysis of these two phenomena it was found that 39% of the viral genome is necessary for the induction of cell DNA synthesis.     

Role of acoustic stress on the development of polyoma tumors in immunized golden hamsters]

An acoustic stress increases the metastatic spread of polyoma virus-induced tumors in syrian Hamsters. To try to elucidate the mechanism of this action, we studied the effect of stress on the protection afforded by the virus against tumour challenge. Exposure to ultrasonics during the immunization period markedly decreased the protective effect of the virus.     

Tumorigenic activity of cloned polyoma virus DNA in newborn rats

Summary The proximal portion of the polyoma virus early region as well as the complete viral genome were cloned in pBR322. Recombinant plasmids induced tumors in newborn rats but only after linearization of the DNA by various restriction endonucleases.This work was financed by grant MA-6731 from the Medical Research Council and by a grant from the National Cancer Institute of Canada.     

In vitro proliferation of human large granular lymphocytes with v-raf/v-myc recombinant retrovirus

The effect of infection with a retrovirus carrying v-raf/v-myc oncogenes (J2 virus) on the in vitro proliferation of human large granular lymphocytes (LGL) was investigated. LGL infected with J2 virus (J2LGL), unlike uninfected cells, grew with a proliferation peak eight days after infection. Such cells retained the morphology and functional properties typical of LGL. Furthermore, 5% of J2LGL produced virus the day after infection, whereas non-virus production was detectable five days later. These data indicate that J2 virus provides a transient mitogenic signal for LGL.     

Presence of autocomplementary RNA with viral specificity in cells infected with herpes virus]

RNA from cells infected with Herpes simplex virus contain a higher percentage of double-stranded RNA than non-infected cells. This percentage increases three-fold upon self-annealing. The complementary RNA sequences were shown to be virus-specific by the following criteria: (1) high melting temperature than double-stranded RNA from non infected cells; (2) higher density in caesium sulphate; (3) specific hybridization with viral DNA.     

Anti-apoptotic mechanisms of HIV: lessons and novel approaches to curing HIV

Past efforts at curing infection with the human immunodeficiency virus (HIV) have been blocked by the resistance of some infected cells to viral cytopathic effects and the associated development of a latent viral reservoir. Furthermore, current efforts to clear the viral reservoir by means of reactivating latent virus are hampered by the lack of cell death in the newly productively infected cells. The purpose of this review is to describe the many anti-apoptotic mechanisms of HIV, as well as the current limitations in the field. Only by understanding how infected cells avoid HIV-induced cell death can an effective strategy to kill infected cells be developed.     

Viral infection associated with mortality in the oyster Crassostrea gigas Thunberg]

Virus particles and their morphogenesis have been observed in the cytoplasm of connective cells in the Japanese Oyster Crassostrea gigas. This virus seems to be similar to those described in the Portuguese Oyster Crassostrea angulata when high rates of mortality were recorded in 1970-1973 and those found in gill disease of this species.     

An increase in Sendai virus-induced cell fusion of erythrocytes infected with Plasmodium chabaudi

The extent of cell fusion induced by Sendai virus was examined in erythrocytes infected with Plasmodium chabaudi. An increase in cell fusion of erythrocytes with Ehrlich tumor cells and of erythrocytes with erythrocytes was observed with the infected erythrocytes. However, agglutination by the virus was not changed between erythrocytes of normal and malarial mice. These results indicate that the increase in cell fusion occurred in the process of membrane fusion, suggesting that some membrane property of Plasmodium-parasitized erythrocytes is changed in terms of Sendai virus-induced cell fusion.     

Induction, by 5-bromo-2'-deoxyuridine, of a "foamy" virus previously undetected in hamster cells transformed by SV40]

TSV5 clone 2 cells in normal conditions of culture contain only an expressed RNA virus (R-type virus). However, exposure of the cells to 5-bromo-2'-deoxyuridine with dexamethasone, induced synthesis of a syncitium-forming ("Foamy") virus. In other hamster cell lines, the same treatment fails to induce a "foamy" virus. The origin of this "foamy" virus is discussed.     

Expression of an antigen associated with Gross virus on the surfaces of murine cells producing an oncornavirus from the radioleukemia of C57BL/6 mice]

A leukemogenic viral complex was demonstrated in cultures of 13-3 C cell line derived from a C57BL/6, radiation leukemia virus (RadLV-Rs) induced tumor. Both 13-3C and leukemic cells induced in C57BL/6 mice by 13-3C virus carry a cell surface antigen associated with Gross leukemia virus (GCSAa). These findings point to a close similarity between these antigens and those of murine endogenous ecotropic viruses.     

Effect of infection of mice with Friend leukemia complex viruses on background antibody-forming cell production in vitro

Summary Friend leukemia complex (FLC) and Rowson-Parr virus (RPV) infections of donor mice depress the production of background antibody-forming cells by splenocytes cultured in the absence of specific antigenic stimulation.Supported in part by a grant from the Italian Research Council (Progetto finalizzato virus, CT 77.00248.84).     

Kristalloide Strukturen im Zytoplasma von lymphatischen Zellen verschiedener Affen

Summary In the endoplasmic reticulum of cells of spleen and lymphnodes of different monkeys, crystalloid inclusions were often found. These inclusions show a pattern of small balls with a diameter of 250 Å, which are connected by 100 Å long bridges. It is supposed that these crystalloid inclusions are produced by the lymphatic cells as a reaction to virus infection, which remains clinically non-apparent, because the same pattern was observed in cells, which were experimentally infected with yellow fever virus, West Nile virus, and rubella virus.     

Mechanisms of heterotypic immunity against canine distemper.

Hep-2 cells infected with measles virus (MV) for as short as 6 h became refractory to superinfection with canine distemper virus (CDV) but not to vesicular stomatitis virus (VSV). The exact mechanism of such interference is unknown but probably occurs after virus attachment and penetration. These results verify the suggestion that virus interference may be a mechanism of heterotypic protection against canine distemper.     

The influence of MuLV and SV40 viruses on senescence in mouse fibroblasts in vitro

Summary Mouse cells productively infected with Moloney leukaemia virus (MuLV) underwent senescence in a manner similar to control cells, although they recovered more readily as an established line. Rapidly growing cell lines were also obtained following simian virus 40 (SV40) infection of senescent cells. However, superinfection of senescent MuLV-producing cells by SV40 led to slower growing cells with a reduced output of infectious MuLV.