Reversion of thermosensitive splicing defect of Moloney murine sarcoma virus ts110 by oversplicing of viral RNA.

Moloney murine sarcoma virus ts110 possesses a thermosensitive splicing defect. By continuously growing nonproducer cells at the nonpermissive temperature, a new class of revertant cells, termed 6m3, that had lost the thermosensitive splicing defect was produced, and six distinct clones were selected. These cell clones were transformed at either permissive or restrictive temperatures.

A common cellular pathway for v-mos and v-Ki-ras is not required for v-Ki-ras-induced tumorigenicity in a nonmalignant, v-mos-expressing revertant cell.

A revertant cell line was selected from Moloney sarcoma virus-transformed BALB/c cells after long-term treatment with type I interferon. Despite an actively transcribed and transfectable v-mos gene, these revertant cells were nontumorigenic in nude mice. The functionality of the mos protein was investigated, focusing on the alpha 2(1) collagen promoter regulation, which is known to be affected by mos-induced trans-acting factors.

Presence of a constitutive paracrine beta-interferon in v-mos-bearing nonmalignant reverted cells.

A stable nonmalignant revertant cell line was derived from Moloney murine sarcoma virus-transformed BALB/c cells after long-term cultivation in the presence of murine type I interferon (IFN). These cells gradually established resistance to exogenous IFN and were also seen to contain IFN-dependent proteins. The presence of an endogenous IFN was confirmed by the results of Northern blot analysis and in situ hybridization with an IFN-beta probe, showing that only mRNA specific for IFN-beta- could be found in the uninduced reverted cells.

Persistent expression of v-mos oncogene in transformed cells that revert to nonmalignancy after prolonged treatment with interferon.

BALB/c embryonic fibroblasts productively transformed by Moloney sarcoma virus and cultivated for over 600 generations in the presence of mouse alpha/beta interferon reverted to an apparently normal phenotype and were unable to produce tumors in nude mice. Nevertheless, the presence of an integrated Moloney sarcoma virus genome in the nonmalignant Moloney sarcoma virus-transformed interferon-treated cell DNA could be shown by focus formation upon transfection and by hybridization with a v-mos probe. After digestion with various restriction endonucleases, similar hybridization patterns of v-mos sequences were obtained with DNAs from both reverted and transformed cells.

Interferon induced by UV-irradiated murine cytomegalovirus decreases type C virus expression in BALB/c cells treated by 5-iodo-deoxyuridine or cycloheximide.

UV-irradiated mouse cytomegalovirus (MCMV) activates at low incidence (2.0 X 10(-4) - 8.0 X 10(-4)) a xenotropic type C virus in Kirsten sarcoma virus-transformed nonproducer BALB 3T3 (KBALB) cells.

Activation of an endogenous mouse type C virus by UV-irradiated murine cytomegalovirus.

Infection of Kirsten sarcoma virus-transformed non-producer BALB-3T3 mouse cells with UV-irradiated mouse cytomegalovirus (MCMV) resulted in activation of a xenotropic type C virus detected by infectious center formation in permissive rat or mink cells. The levels of type C virus activated by MCMV were related to the UV dose applied. Under optimal conditions the frequencies of activation varied from 3.

Isoprinosine delays the early appearance of autoimmunity in NZB/NZW F1 mice treated with interferon.

NZB/NZW F1 hybrid mice treated for long periods with type beta interferon developed early symptoms of autoimmune disease. In these animals the level of anti-dsDNA antibody begins to increase at 4-6 months while untreated NZB/NZW mice do not display similar levels until 12 months. The concomitant administration of isoprinosine and interferon delays the early appearance of autoimmune disorders.

Adverse effects of interferon treatment on the life span of NZB mice.

NZB mice treated with interferon from birth and for over a year, display early some characteristics of the autoimmune disease. In these animals, mortality is clearly higher than in controls. Their death occurs 3 to 6 months before that of mice injected with a "mock" preparation.

[A search for viruses in systemic lupus erythematosis. Somatic fusion amoung mammalian cells using concanavalin A].

Attempts were made to isolate a virus from systemic lupus erythematosus patients, using lymphocyte cultures prepared from peripheral blood. Both cocultivation with VERO cells and fusion experiments in which lysolecithin and Concanavalin A were employed as fusing agents failed to reveal any presence of virus. Con A proved to be useful for heterokaryon formation in primate cells, fusion levels varying from 14-21% as shown by autoradiography.

Recombination between guanidine-resistant and dextran sulfate-resistant mutants of type 1 poliovirus.

Mixed infection of monkey kidney cells with two mutants of the LSc2ab strain of poliovirus, one resistant to guanidine and the other resistant to both dextran sulfate and 2-(alpha-hydroxybenzyl)-benzimidazole (HBB), yielded progeny in which the number of gua(r)dex(r) particles exceeded by a factor of 7 to 10 the expected number of similar particles occurring through spontaneous mutation; recombination would explain the fairly high excess of doubly mutant particles that was obtained. Scoring of HBB resistance in 50 gua(r)dex(r) clones suggested that, during recombination, resistance to dextran sulfate is not associated with HBB resistance.