Biomedical subjects
Publications and source records attributed to J V Hallum.
Prolonged treatment with relatively high concentrations of interferon was required to "cure" L cells persistently infected with Newcastle disease virus.
Eagle's medium adjusted to pH 6 was found to inhibit the rate of RNA and protein syntheses in monolayer cultures of L cells. Incubation of the cells at pH 6 decreased the rate of incorporation of amino acids into nascent peptide chains and caused a disaggregation of polyribosomes. Messenger RNA seemed to persist during the exposure of the cells to medium adjusted to pH 6, since protein synthesis resumed when the cells were transferred to recovery medium containing actinomycin D. The inhibitory effects of pH 6 on macromolecular synthesis were reversible and the viability of the cells exposed to pH 6 did not decrease. The permeability of the cells was not altered by the exposure to pH 6.
When the sensitivities to interferon of Newcastle disease virus (NDV) and vesicular stomatitis virus (VSV) were compared by the plaque reduction method in chick embryo cell cultures, NDV was found to be 45-fold more resistant than VSV. This difference was exaggerated when a multiple-cycle yield inhibition method was employed. In marked contrast, when the same viruses were tested by a single-cycle yield inhibition method, the difference in sensitivity to interferon of the two viruses was virtually eliminated. Further investigation showed that, in chick embryo cells exposed to interferon, the resistance to NDV decayed more rapidly than resistance to VSV. This finding explained the divergent results obtained with the two viruses when single- or multiple-cycle replication techniques were employed. Experiments carried out with L cells showed that cellular antiviral resistance decayed much more slowly in these cells than in chick embryo cells. Consequently, when measured by the plaque reduction method in L cells, no difference was observed in the sensitivity to interferon of VSV and NDV(pi), a mutant of NDV which replicates efficiently in L cells. A procedure is suggested for determining the relative sensitivities to interferon of different viruses under conditions which minimize the role of decay of antiviral resistance in the host cells.
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The pH of the solution in which interferon was applied to L cells determined the level of resistance developed against challenge with vesicular stomatitis virus (VSV). No inhibition of challenge virus was observed when interferon was applied to cells at pH 6.0. At pH 6.5, partial inhibition of VSV replication was observed and inhibition was maximum at pH 7.0. Evidence was obtained that interferon interacted with L cells at pH 6.0, but that resistance did not develop until the cells were placed in a medium at pH 7.0. These effects were explained by data showing that exposure of cells to a medium at pH 6.0 reversibly inhibited both ribonucleic acid and protein synthesis.
Hallum, J. V. (University of Pittsburgh, Pittsburgh, Pa.), and J. S. Youngner. Urea and thermal mutants of poliovirus. J. Bacteriol. 91:2305-2308. 1966.-Thermally selected mutants of poliovirus which differed in sensitivity to heating at 50 C were inactivated with urea. With 3 m urea, urea resistance paralleled thermal resistance. In contrast, when urea-resistant mutants were selected from thermosensitive, urea-sensitive, wild-type poliovirus, the 50 C sensitivity of the selected mutants did not change. These findings indicate a lack of covariance of the urea and the 50 C-inactivation markers of poliovirus.
Hallum, J. V. (University of Pittsburgh, Pittsburgh, Pa.), and J. S. Youngner. Quantitative aspects of inhibition of virus replication by interferon in chick embryo cell cultures. J. Bacteriol. 92:1047-1050. 1966.-The effect of interferon on single cycles of replication of vesicular stomatitis virus and Mahoney poliovirus ribonucleic acid was studied in chick embryo cell cultures. The results showed that the titer of a given interferon preparation was independent of the input multiplicity of the challenge virus. In addition, the increase in virus yield with increasing virus challenge was a function of the number of infected cells, each of which yielded progeny at a level determined by the concentration of interferon to which the cells were exposed. These findings are not compatible with the concept that increases in the size of the virus challenge reverse or overcome protection of cells by interferon.
Youngner, Julius S. (University of Pittsburgh, Pittsburgh, Pa.), Anne W. Scott, Jules V. Hallum, and Warren R. Stinebring. Interferon production by inactivated Newcastle disease virus in cell cultures and in mice. J. Bacteriol. 92:862-868. 1966.-A comparison was made of the effects of ultraviolet (UV) irradiation or heating at 56 C on the interferon-stimulating capacity of Newcastle disease virus in primary chick embryo fibroblast (CE) cultures, in L-cell cultures, and in the intact mouse. The data obtained indicated the critical importance of the host cell system used for interferon production. Virus inactivated by UV irradiation, as well as infective virus, was an effective stimulus of interferon production in L cells and in mice, and this property persisted on continued irradiation. In contrast, in CE cell cultures, infective virus produced no interferon, whereas UV-irradiated virus produced maximal interferon titers when all infectivity was destroyed; continued irradiation resulted in a rapid loss of the interferon-stimulating capacity of the virus. Virus inactivated at 56 C did not produce interferon in CE or L-cell cultures. In the intact mouse, on the other hand, heat-inactivated virus was capable of stimulating the release of significant levels of circulating interferon.
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