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C J Gauntt

Publications and source records attributed to C J Gauntt.

63 records · Page 4Linked to original sources
PubMed1975

Properties and origins of infectious rhinovirus type 14 particles of different buoyant densities.

Isopycnic centrifugation of rhinovirus type 14 (RV14), purified from infected HeLa or KB cell cultures, into CsCl gradients resolved two bands of infectious virus particles with buoyant density values of 1.409 +/- 0.007 (H virus) and 1.386 +/- 0.004 (L virus) g/ml. Only H virus was detected by incorporation of radiolabeled uridine into viral RNA, and H virus accounted for the majority of infectivity in gradients. H and L virus could not be differentiated by plaque morphology, extent of neutralization by RV14-specific antiserum, or particle size. Electron microscope studies showed that most L-virus particles were associated with an amorphous material. Treatment of L virus with proteolytic enzymes or rebanding L virus in CsCl gradients resulted in recovery of the majority of infectivity as H virus. Virus purified from cell-free fluids from infected HeLa or KB cell cultures banded only as H virus. HeLa cell cultures challenged with purified H virus and harvested at 3 h postinoculation for virus purification yielded only infectious H virus. Both H and L viruses were detected in cell cultures that had been challenged with purified H virus and harvested at 12 h postinoculation. The data suggest that H virus represents progeny virus, whereas L virus represents sequestered infectious virus particles which become associated with an amorphous material and do not enter into viral replicative processes.

Adsorption↗
PubMed1973

Induction of interferon in L cells by reoviruses.

L cell cultures challenged with reoviruses types 1 and 3 produced little to no detectable interferon under conditions which permitted virus replication and under conditions which prevented replication of a temperature-sensitive mutant strain of reovirus type 3 (ts-1). Ultraviolet-irradiated reoviruses and double-stranded ribonucleic acids extracted from purified reovirus type 3 also induced little to no interferon in L cell cultures. Under similar conditions, MM virus proved to be an effective inducer of interferon. Exposure of L cells to interferon prior to challenge with virus (priming) failed to enhance interferon production upon subsequent challenge with reovirus although priming increased the amount of interferon produced following MM virus challenge. L cell cultures that were challenged with reovirus type 3 and subsequently with either MM or Colorado tick fever viruses produced similar titers of interferon as cell cultures that were challenged with either MM or Colorado tick fever virus alone, respectively. These data show that the presence of production of reovirus type 3 double-stranded ribonucleic acid is not sufficient for induction of interferon in L cell cultures and that additional processes which are required for induction of interferon in L cell cultures are not expressed by reovirus type 3.

Interferons↗
PubMed1968

Transcription of the genomes of type 1 and type 3 reoviruses.

The double-stranded ribonucleic acid (RNA) genome of type 1 reovirus was fragmented into three size classes on extraction, as has already been shown for reovirus type 3. The relative amounts and molecular weights of the three classes were the same for the two viruses. Cells infected with type 1 virus synthesized three classes of messenger RNA. Each class of messenger RNA hybridized exclusively with a denatured double-stranded RNA fragment of equivalent length, as had also been found for type 3 reovirus. The double-stranded RNA segments thus act as specific units for transcription of messenger RNA in the infected cells. In cells infected with type 3 reovirus, the three classes of messenger RNA are made in equal amounts throughout the course of multiplication. In contrast, cells infected with type 1 virus produced only half as much of the largest messenger RNA as they did of the other two classes at all times during the replicative cycle. This finding suggests that transcription of the largest segments of type 1 viral genome is restricted.

Animals↗
PubMed1968

Destruction of L cells by Mengo virus: use of interferon to study the mechanism.

Interferon, when added to L cells, inhibited the synthesis of infectious Mengo viral ribonucleic acid, hemagglutinins, and infectious virus by 85 to 95%. Serum-blocking antigens were also reduced by the action of interferon, but threefold excess amounts of these antigens accumulated in interferon-treated cultures above the amounts expected for the quantity of infectious virus that was produced in these cultures. Radioautographic analysis showed that 28 to 36% of the cells of an interferon-treated population synthesized viral ribonucleic acid and 36 to 47% produced viral antigens as determined by an immunofluorescence technique. Despite the reductions in synthesis of viral components, all cells in an interferon-treated culture underwent cytopathic effects at the same time as cells in infected cultures which had not been treated with interferon. The results are compatible with the hypothesis that the cell destruction which results from the infection of L cells with Mengo virus is due to a protein which is coded for by the virus but is not a component of the mature virion.

Animals↗
PubMed1968

Reovirus-induced ribonucleic acid polymerase.

A virus-induced ribonucleic acid (RNA) polymerase activity was found in L cells infected with type 3 reovirus. Most of the enzyme is associated with the "large particle" fraction of the infected cells. The enzyme first appeared at 3 to 5 hr after infection and increased in amount until 7 to 9 hr. All four ribonucleoside triphosphates are incorporated in vitro into an acid-insoluble form by the enzyme. The major part of the product formed in vitro is a double-stranded RNA indistinguishable from viral RNA by electrophoresis on polyacrylamide gel. Approximately 40% of the product is a single-stranded RNA of relatively small molecular weight. More than 95% of the nucleotides incorporated into double-stranded RNA by the enzyme are bound in internal 3'-5'-phosphodiester linkages extending back from both 3'- and 5'-termini of the RNA strands.

Acrylates↗
PubMed1966

Inhibition of Mengo virus by interferon.

Gauntt, Charles J. (The University of Texas, Austin), and Royce Z. Lockart, Jr. Inhibition of Mengo virus by interferon. J. Bacteriol. 91:176-182. 1966.-The inhibition of Mengo virus replication in L cells resulting from interferon was studied quantitatively. Interferon was titrated on L cells with Western equine encephalomyelitis (WEE) virus as the challenge virus. One protective unit (PU) of interferon is the least amount of interferon which prevents cytopathic effects when a large multiplicity of WEE virus is added subsequent to overnight incubation with interferon. Ten PU of interferon reduced the yields of Mengo virus by about 90%. Larger doses of interferon, up to 220 PU, caused no further reduction in the amount of virus produced. Plaque formation by Mengo virus was also reduced in number by about 85 to 90%, but could not be further reduced. The plaques which formed on interferon-treated cells were reduced in size. We were unable to obtain a virus population with increased resistance to interferon action by use of five successive growth cycles in interferon-treated cultures. Analysis of the cell population for the proportion of cells able to act as infectious centers revealed that incubation of cells with 10 PU of interferon decreased the proportion of virus-yielding cells by 80%. The yield of virus per virus-producing cell was decreased by 40 to 60%. Despite the reduction in yields, plaques, and infectious centers resulting from interferon, all doses of interferon failed to prevent the complete destruction of the cells. Experiments with puromycin indicated that the cytopathic effects observed in L cells infected with Mengo virus required that a virus-directed protein be synthesized between 4 and 5 hr postinfection. The evidence suggested, therefore, that the Mengo virus genome was able to code for new protein synthesis in the absence of the production of infectious virus.

Cytopathogenic Effect, Viral↗