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Biomedical subjects

H B Levy

Publications and source records attributed to H B Levy.

At least 109 records · Page 6Linked to original sources
PubMed1969

Inhibition of tumor growth by polyinosinic-polycytidylic acid.

The synthetic double-stranded RNA, polyinosinic-cytidylic acid, inhibits the growth of some tumors in mice. Two days after implantation of a reticulum cell sarcoma, a lymphatic lymphoma, a fibrosarcoma, two leukemias, and a human adenovirus 12-induced tumor, treatment of groups of mice resulted in decreased growth rates of the tumors and increased survival times of the animals. In the two tumors tested (the reticulum cell sarcoma and the adenovirus 12-induced tumor) initiation of treatment after the tumor was grown to moderate size caused a regression of the tumor. In the case of the reticulum cell sarcoma, the tumor had not reappeared in some of the animals two months after cessation of treatment.

Adenoviridae↗
PubMed1969

Induction of interferon by preparations of synthetic single-stranded RNA.

A study was undertaken to help determine whether synthetic nonbase-paired, single-stranded RNA as well as synthetic base-paired, double-stranded RNA could induce interferon. Synthetic polyriboinosinic acid and polyribocytidylic acid induced interferon and interferon-like resistance in several different cell culture systems. However, in the intact rabbit only the most active preparations of single-stranded RNA induced circulating interferon when injected intravenously. The induced interferon and antiviral effect in tissue culture and animals was shown to have characteristics of the interferon system. Contamination of the single-stranded synthetic RNA materials by small amounts of base-paired, double-stranded RNA was ruled out by failure to find sufficient heterologous nucleic acid bases by differential activities of single-stranded and double-stranded RNA's in different cell systems and by failure to detect double-stranded RNA in poly-rI upon chromatography on benzoylated DEAE-cellulose.

Animals↗
PubMed1967

Ribosomes: effect of interferon on their interaction with rapidly labeled cellular and viral RNA's.

Rapidly labeled RNA of mouse L cells and labeled RNA of Mengo virus, unlike cellular RNA labeled under steady-state conditions, form detectable complexes with L-cell ribosomes. These ribosome-RNA complexes formed in vitro appear analogous to those assembled during polysome formation in vivo. When ribosomes are prepared from L cells exposed to homologous interferon, their capacity to associate with cell messenger is preserved, while their ability to interact with viral RNA is markedly reduced. The ribosomes from cells exposed to interferon are thus altered selectively to permit only certain messages to be bound and translated.

Animals↗
PubMed1967

Interferon action on parental Semliki forest virus ribonucleic acid.

Actinomycin D-treated chick fibroblasts were infected with purified (32)P-labeled Semliki forest virus, and ribonucleic acid (RNA) was extracted after 1 or 2 hr. Within 1 hr, viral RNA forms sedimenting in sucrose gradients at 42S, 30S, and 16S were present. The 42S form corresponded to the RNA of the virion. The 16S form appeared to be a double-stranded template for the formation of new viral RNA, since nascent RNA was associated with it and the molecule could be heat-denatured and subsequently reannealed by slow cooling. Interferon treatment before infection, or puromycin (50 mug/ml) or cycloheximide (200 mug/ml) added at the time of virus infection, had no effect on the formation of the 30S RNA but inhibited the production of the 16S form. Several findings made it unlikely that these results were due to breakdown of parental RNA and reincorporation of (32)P into progeny structures. The results suggested that the mechanism of interferon action involves inhibition of protein synthesis by parental viral RNA, since a specific viral RNA polymerase had previously been demonstrated to be necessary for production of 16S RNA. No protein synthesis appears necessary for formation of 30S RNA from parental virus RNA.

Animals↗