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Biomedical subjects

C Altaner

Publications and source records attributed to C Altaner.

At least 73 records · Page 4Linked to original sources

The cell-growth inhibitory effect of interferon. Studies of a resistant cell-subline.

Studies performed in the CSV subline of mouse L-cells suggest that activated endogenous and/or exogenous viral infection might be the factor that modifies the cell surface and, in consequence, the sensitivity of the cell to the cell-growth inhibitory action of interferon. In contrast with the parental L-cells, the CSV subline obtained by prolonged passage of L-cells in the presence of interferon shows an altered electron microscopic morphology, absence of C type particles and a decreased agglutinability with Concanavalin A. It is resistant to the cell-growth inhibitory effect of interferon but retains the sensitivity toward its antiviral effect. However, the sensitivity of the CSV subline toward the cell-growth inhibitory effect of interferon increased significantly after treatment with 5-iododexyuridine, infection with the Harvey strain of mouse sarcoma virus and/or prolonged passages in vitro. In this respect, the CSV subline resembles the primary mouse embryonic cells. Since sensitivity of CSV cells increased also after treatment with cyclic 3'-5' adenosine monophosphate and/or prostaglandin E2, it is possible that the cell-growth inhibitory effect of interferon is mediated through the "second messenger" system.

Animals↗

DNA polymerase activity and antibody against it in sera of patients with systemic lupus erythematosus.

In the sera of one half of patients with sytemic lupus erythematosus (SLE) the endogenous and exogenous DNA polymerase activities were observed. The simultaneous presence of DNA polymerase activity and the antibodies to denatured DNA in the half of polymerase positive SLE sera was proved. The polymerase activity was not associated with virus-like particles. The endogenous polymerase activity probably used RNA, the exogenous one prefered DNA as a template. The determination of template requirement was complicated by the complexity of SLE sera. The product of polymerase activities were DNA-RNA hybrid and DNA. In some sera of the SLE patients without polymerase activity the antibodies against the polymerase were found. The occurrence of DNA polymerase activity and possible viral origin of SLE was discussed.

Antibodies↗

Suppression of the avian sarcoma virus genome in 8-azaquanine-resistant, transformed, hamster cells.

The avian sarcoma virus genome (Schmidt-Ruppin strain) in transformed hamster cells resistant to 8-azaquanine [Ha(SR)AG-50] was strongly suppressed. The suppression was genetically stable and could not be overcome by attempts at induction with 5-iodo-2'-deoxyuridine. Fusion of hamster cells, which had suppressed virus genome, with chicken Rous-associated virus (RAV-1)-preinfected cells easily rescued the sarcoma virus. The rescued virus had envelope properties of RAV-1, as determined by viral interference, virus neutralization, and plating on genetically resistant chicken cells. By repeatedly cloning the rescued virus, we determined that virus recombined in the rescue experiment and that the recombinant virus had the envelope properties of helper virus used for its rescue. Cells with suppressed avian sarcoma virus genome were suitable for preparation of different recombinant viruses.

Animals↗

Infection of human embryo cells with avian sarcoma virus B77 in vitro.

Human embryo cells were infected with avian sarcoma virus B77--Hu(B77). The virus genome was detected in the Hu(B77) cells during subsequent cell passages in the uncloned cells as well as in single-cell clones. Despite the presence of the virus genome in cells, the growth properties did not differ from uninfected cells. The Hu(B77) cells did not reveal the transformed phenotype in vitro.

Avian Sarcoma Viruses↗

Mouse MSV transformed cells resistant to 8-azaguanine.

Mouse cells transformed by murine sarcoma virus were made resistant to 8-azaguanine. Resistant cells and cell clones isolated from them were deficient in hypoxanthine-guanine phosphoribosyl transferase (HGPRT) activity. They did not grow in HATG medium, did not incorporate labeled hypoxanthine, and had negligible HGPRT activity. The resistance was genetically stable. The resistant cells were hyperdiploid and contained telocentric chromosomes only. The resistant cells as well as the progenitor cells were slightly tumorigenic in mice, the plating efficiency in soft agar was very low. The parental cells and aza-G resistant cells produced C-type viral particles having RNA-dependent DNA polymerase activity. The resistance to aza-G did not influenced the expression of murine sarcoma virus genome in cells. The resistant cells are suitable for preparation of cell hybrids.

Animals↗

Transformation of rat liver cells with chicken sarcoma virus B77 and murine sarcoma virus.

Rat liver cells in vitro were transformed with chicken sarcoma virus B77, giving RL(B77) cells, and with murine sarcoma virus (Harvey), giving RL(MSV) cells. Rat liver cells transformed spontaneously in vitro were designated RL cells. In addition, the RL(MSV) cell line was adapted for growth in culture fluid containing 25 mug of 5-bromodeoxyuridine per ml. All cell lines were tumorigenic in 1-wk-old rats. The number of cells needed for induction of tumor growth was 1,000-fold higher in the case of RL(B77) cells in comparison with RL(MSV) cells and RL cells. No production of viral particles from any of the cell lines investigated was detected by plating concentrated supernatant fluid of the cultures on different secondary embryo cells with and without fusion by Sendai virus, by labeling with uridine-5-(3)H, or by assay for deoxyribonucleic acid polymerase activity. The viral genome was rescued by fusion of RL(B77) cells with chicken cells. Chicken sarcoma virus rescued from (RL(B77) cells differed in plating efficiency on duck cells from B77 virus rescued from transformed rat embryo cells. No virus was rescued after fusion of RL(MSV) and RL cells with mouse, rat, or chicken embryo cells. Infectious murine sarcoma virus can be induced by 5-bromodeoxyuridine from RL(MSV) cells.

Alpharetrovirus↗