Shipman, Charles Jr. (Indiana University School of Medicine, Indianapolis), and Alvin S. Levine. Selective response of the Japanese quail to various strains of Rous sarcoma virus. J. Bacteriol. 92:161-163. 1966.-The Bryan "high-titer," Carr-Zilber, Harris, Prague, Schmidt-Ruppin, and "29" strains of Rous sarcoma virus were used to initiate tumors in the Japanese quail (Coturnix coturnix japonica). Although all strains produced tumors upon primary inoculation, only the Bryan "high-titer" and Harris strains could be serially passaged with cell-free tumor extracts. Analysis by means of the end-point dilution technique and the interference test revealed that the tumor extract of the Bryan "high-titer" strain passaged 10 times in the quail contained a Rous-associated virus.

Animals↗

PubMed1965

Tumor production in the Japanese quail by the Schmidt-Ruppin strain of Rous sarcoma virus.

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Animals↗

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Serologic and karyologic evidence of incorrect identity of an animal cell line (guinea pig spleen).

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Animals↗

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A three-dimensional model to analyze drug-drug interactions.

Nearly four generations of investigators have studied combined drug effects. Their methods of generating and analyzing data have changed dramatically over the years but the basic problem has not. This review examines the inherent difficulties in analyzing combined drug effects and evaluates modern methods of describing these interactions. Researchers have traditionally used two-dimensional (2-D) methods to approximate the actual three-dimensional (3-D) nature of drug interactions. We conclude that these 2-D methods are often inadequate when used to analyze synergistic and antagonistic drug interactions in antiviral and anticancer chemotherapy. We propose a direct and pragmatic 3-D approach to the problem, made possible by microcomputers and sophisticated graphics programs. This procedure directly elucidates the shape of the dose-response surface, identifies the regions of statistically significant synergy and antagonism, and quantitates these effects. It also greatly simplifies the problem since a 3-D surface presents complete drug interactions in a way that can be easily interpreted. We will show that understanding the shape of the resulting 3-D surface is essential to an understanding of complex drug interactions. This new method facilitates the rigorous analysis of drug-drug interactions and offers investigators powerful new tools to analyze combinations of antiviral and anticancer drugs.

Antiviral Agents↗

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Ribonucleotide reductase: an important enzyme in the replication of herpes simplex virus type 1 and a target for antiviral chemotherapy.

Herpes simplex virus encodes a ribonucleotide reductase that catalyzes the formation of deoxyribonucleotides from ribonucleotides. The enzyme is not essential for either viral DNA synthesis or replication, yet inhibitors of this enzyme suppress viral replication. To clarify the role of the ribonucleotide reductase in virus infection and to evaluate it as an antiviral target, the metabolism of deoxyribonucleotides in infected cells was examined. Our results show that the cellular ribonucleotide reductase is incapable of generating adequate deoxyribonucleoside triphosphate pools to support efficient virus replication. Additionally, we have shown that the virus is unable to efficiently utilize salvaged deoxyribonucleosides from degraded cellular DNA. A selective inhibitor of the viral ribonucleotide reductase, 2-acetylpyridine thiosemicarbazone, decreased deoxyribonucleotide pools in infected cells, thus inhibiting viral DNA synthesis. This compound also inhibited the cellular ribonucleotide reductase to some extent, thereby enhancing its antiviral activity. The antiviral effects of acyclovir were potentiated by 2-acetylpyridine thiosemicarbazone in the wild-type virus but not in the ribonucleotide reductase mutant, ICP6 delta. Collectively, these data strongly suggest that the viral ribonucleotide reductase is an important enzyme in viral replication and a valid target for antiviral chemotherapy.

Acyclovir↗

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