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B W Mahy

Publications and source records attributed to B W Mahy.

71 records · Page 4Linked to original sources
PubMed1972

Inhibition of influenza virus replication by -amanitin: mode of action.

The replication of influenza virus in chick embryo fibroblast cells is inhibited by alpha-amanitin added during the first 2 hr of infection at concentrations similar to those required to inhibit cellular DNA-dependent RNA polymerase form II in vivo. Of two periods of increased RNA synthesis observed in cells infected with influenza virus, only the first, occurring from 0 to 2 hr after infection, is sensitive to alpha-amanitin. During this early period, there is a stimulation of the activity of DNA-dependent RNA polymerase II of nuclei isolated from infected cells. The data suggest that DNA transcription mediated by polymerase II is essential for influenza virus replication.

Animals↗
PubMed1970

Ribonucleic acid polymerase induced in cells infected with Sendai virus.

A ribonucleic acid (RNA)-dependent RNA polymerase was induced in chick embryo fibroblast cells after infection with Sendai virus (parainfluenza 1 virus). The enzyme was associated with the microsomal fraction of infected cells and reached maximum detectable activity at 18 hr after virus infection. The activity of the enzyme in vitro was dependent on the presence of added magnesium ions and all four nucleoside triphosphates and was not inhibited by actinomycin D. The RNA synthesized by the enzyme in vitro was sensitive to ribonuclease and consisted of a complex mixture of RNA species including 34S, 24S, and 18S components. Similar RNA components were detected in the microsomal fraction of Sendai virus-infected cells by labeling with (3)H-uridine from 17 to 18 hr postinfection in the presence of actinomycin D. Of the RNA synthesized by Sendai virus-induced RNA polymerase in vitro, 98% became insensitive to ribonuclease after annealing with RNA extracted from purified Sendai virus particles.

Animals↗
PubMed1970

In vitro product of a ribonucleic acid polymerase induced by influenza virus.

The ribonucleic acid (RNA)-dependent RNA polymerase induced in the microsomal fraction of cells infected with influenza virus synthesized a mixture of single-and double-stranded RNA in vitro. The single-stranded RNA sedimented mainly in the 8S region on sucrose density gradients, with a smaller proportion of the RNA sedimenting at 18S. This sedimentation pattern corresponds closely to that of incomplete influenza virus RNA. The double-stranded RNA formed in vitro sedimented at 11S, but molecules which may be replicative intermediate, sedimenting at 14 to 20S, were also detected in the in vitro reaction product. Similar species of RNA were detected in vivo by pulse-labeling infected cells at the time of polymerase harvest, but the proportion of each RNA species was different, most of the RNA being single-stranded and sedimenting in the 18S region. An 11S double-stranded RNA was also synthesized in vivo. Pulse chase analysis of the double-stranded RNA synthesized in vitro showed that most is stable, and only a small proportion turns over during the reaction. A proportion of the RNA formed in vitro could be annealed to RNA formed in infected cells and to RNA extracted from purified virus.

Animals↗
PubMed1968

Deoxyribonucleic acid-dependent ribonucleic acid polymerase activity in cells infected with influenza virus.

Deoxyribonucleic acid (DNA)-dependent ribonucleic acid (RNA) polymerase activity was assayed on nuclear preparations of chick embryo fibroblast cells at various times after infection with an influenza A virus (fowl plague virus) and was compared with the activity of uninfected cells. Polymerase activity was increased by about 60% by 2 hr after infection, and this increase coincided with an increase in RNA synthesis in infected cells, as determined by pulse-labeling with uridine. No difference could be detected between the polymerases of infected and uninfected cells as to their requirements for DNA primer, divalent cations, and nucleoside triphosphates, and they were equally sensitive to addition of actinomycin D to the reaction mixture. It is possible that host cell DNA-dependent RNA polymerase is involved in the replication of influenza virus RNA.

Animals↗
PubMed1967

Studies on the mechanism of action of Riley virus. IV. The reticuloendothelial system and impaired plasma enzyme clearance in infected mice.

The plasma clearance of intravenously injected rabbit muscle LDH was studied. In normal mice the clearance followed a biphasic exponential curve comprising an initial fast and subsequent slow phase. Riley virus-infected mice showed only the slow phase of enzyme clearance. The change from fast to slow clearance rate in normal mice appeared to depend upon the level of plasma enzyme activity rather than on the amount of enzyme cleared. Treatment of mice with RES-blocking agents (cholesterol oleate and carbon) inhibited the fast clearance phase, whereas an RES-stimulating agent (stilbestrol) caused an accelerated rate of enzyme clearance. Riley virus infection was found to inhibit the clearance of phosphoglucose isomerase, but had no effect on the clearance of alanine transaminase. The activity of the former enzyme is raised in the plasma of infected mice, whereas the activity of the latter enzyme is unaltered.

Alanine Transaminase↗
PubMed1965

Studies on the mechanism of action of Riley virus. I. Action of substances affecting the reticuloendothelial system on plasma enzyme levels in mice.

Plasma LDH levels were determined in normal and Riley virus-infected mice following treatment with various drugs known to alter the activity of the RES. The rise in plasma LDH level after Riley virus infection was considerably enhanced by previous treatment with thorotrast (to produce blockade of the RES), and decreased by previous treatment with stilboestrol (to stimulate the RES). A dose of 2000 r whole-body x-irradiation, lethal within 3 to 4 days, did not alter the phagocytic activity of the RES, and was without effect on plasma LDH activity in normal mice, or on the rise in plasma LDH level following infection with Riley virus. Blockade of the RES with cholesterol oleate, thorotrast, or zymosan, resulted in a 2- to 3-fold rise in plasma LDH level within a few hours. The level returned to normal by 1 to 3 days. Stimulation of the RES with stilboestrol resulted in a decrease in plasma LDH level by 1 to 2 days in both normal and infected mice, with a return to normal by about a week. Blockade of the RES in uninfected mice with thorotrast or cholesterol oleate, besides increasing the plasma LDH level caused a rise in plasma phosphoglucose isomerase level, but no significant alterations in plasma aldolase or alanine transaminase levels, studied up to 10 days. Riley virus causes a similar pattern of enzyme elevation. It is suggested that the increased levels of certain plasma enzymes in Riley virus-infected mice may be due to competitive inhibition by virus particles of plasma enzyme clearance by the RES.

Alanine Transaminase↗
PubMed1965

Studies on the mechanism of action of Riley virus. II. Action of substances affecting the reticuloendothelial sysem on the level of viraemia.

The level of viraemia was determined in serial blood samples obtained from 2 mice after the injection of Riley virus. The plasma virus titre rose rapidly to a peak value of 10(9) to 10(10)ID(50) per ml by 24 hours after infection, and then fell slowly to a level of 10(5) to 10(6)ID(50) per ml by the 10th day after infection, where it remained relatively stable. Neither blockade of the RES with thorotrast, zymosan, or carbon, nor stimulation of the RES with stilboestrol or zymosan, before the injection of Riley virus, produced any observable alteration in the level of viraemia attained 24 hours after infection. However 10 days or more after infection with Riley virus blockade of the RES with thorotrast caused a transitory rise, and stimulation of the RES with stilboestrol caused a slight but prolonged fall, in the level of viraemia. Zymosan injection at this period of infection caused an initial rise, followed by a fall, in the level of viraemia; these changes correlated with the initial period of blockade and the subsequent period of stimulation of the RES observed in carbon clearance studies. The clearance of injected Riley virus particles from the plasma over a period of 3 hours after injection was measured in previously uninfected mice and mice which had been infected with Riley virus for 3 weeks. The mice which had been infected 3 weeks before the test cleared rather more of the injected virus than the previously uninfected mice. It is concluded that although the activity of the RES affects, and may determine, the level of viraemia, the permanence of the viraemia in Riley virus-infected mice does not appear to be due to a failure of the RES to clear virus particles from the plasma.

Animals↗