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At least 325 records · Page 18Linked to original sources
PubMed1983

Isolation and genetic characterization of temperature-sensitive mutants that define five additional recombination groups in simian rotavirus SA11.

Nineteen independent temperature-sensitive (ts) mutants were isolated from SA11 following mutagenesis with proflavin or 5-azacytidine. Fourteen of the ts mutants fell into one or another of five mutant groups previously defined by recombination. Five of the ts mutants defined five recombination groups (F, G, H, I, and J) that had not been previously identified. Thus, 10 of the 11 expected mutant groups have been identified in SA11. The prototype mutants of the 10 mutant groups were tested for recombination at nonpermissive temperature to determine if any group had a lesion affecting recombination. Most mutant pairs recombined efficiently; however, the tsH mutant was restricted in its recombination with the tsB and tsI mutants and the tsG and tsJ mutants failed to recombine at detectable levels at nonpermissive temperature. The mutants of groups F-J did not complement, or did so inefficiently, and interfered with the growth of wild type at both permissive and nonpermissive temperatures. The growth properties of the mutants of groups F-J are described.

Animals↗
PubMed1983

Defective interfering particles of Sendai virus modulate HN expression at the surface of infected BHK cells.

The expression of the Sendai viral glycoproteins HN and F0 at the surface of BHK 21 cells was studied during infection with standard virus, with a mixture of standard and defective interfering (DI) particles (mixed virus infection), and during persistent infection. It is shown that by 2 days after infection, the expression of the HN protein at the surface of mixed virus-infected cells is reduced compared to that observed on standard virus-infected cells as estimated by cell surface immune precipitation of iodinated proteins. This reduced expression results from a reduced efficiency of HN insertion in the plasma membrane, as well as from the inaccessibility to antibody of part of the HN present at the membrane. The HN protein is also poorly expressed at the surface of persistently infected cells, originally infected with a mixture of DI and standard virus particles. In contrast, the expression of the F0 protein at the surface of the infected cells is similar regardless of the type of infection.

Animals↗
PubMed1983

Nongenetic complementation in VSV: asymmetric contribution of the L proteins of each parent in the rescue of group I ts mutants.

Complementation group I temperature-sensitive mutants of vesicular stomatitis virus (VSV) are rescued at nonpermissive temperature by UV-irradiated virus. Rescue is a nongenetic process mediated by the structural L protein molecules of the parental irradiated virus. This is shown by action spectra analysis (V. Deutsch, B. Muel, and G. Brun (1977), Virology 77, 294-305), efficiency of rescue at doses high enough to inactivate every gene I, and rescue by irradiated defective-interfering short particles. Viral molecular synthesis at 39.6 degrees using the ts genomes as templates and stimulated by UV-irradiated virus is shown by gel electrophoresis of rescued virion proteins. Parental strain ts 053(I) is thermolabile in vitro while the thermostability of the rescued virions, genetically characterized as ts group I virus, is identical to that of helper wt or ts+ revertant. This suggests that some parental Lwt molecules are reincorporated in the rescued virions, together with newly synthesized Lts molecules. Efficiency variation of the rescue as a function of the multiplicity of infection of the UV-irradiated virions depends on the m.o.i. of the unirradiated ts I mutants. This result suggests that rescue depends on the concentration of the helper L molecules and also of that of the L initially bound to the ts template. That L of both parents contribute to rescue is supported by the observations that (1) rescue by UV-wt is strongly diminished after in vitro heating of thermolabile ts O53(I). (2) Intragenic rescue can be demonstrated: The helper activity of a given UV-ts I mutant is different according to the unirradiated ts I mutant used; the activity of helper L associated with different templates in intragenic heterologous combinations is higher or lower than its activity in the homologous combination (self-rescue control), instead of being equal as expected. (3) Efficiency of rescue by UV-wt also varies according to the ts I mutant. The initially bound Lts seems therefore to play a role important and different from that of the helper L. Contribution of both parent L to rescue seems thus to be qualitatively different.

Animals↗
PubMed1984

Defective interfering particles of mouse hepatitis virus.

After six to eight serial undiluted passages of mouse hepatitis virus (JHM strain) in DBT cell culture, a decrease in the yield of infectious virus occurred, and with further passages fluctuating yields of infectious virus were observed. The serially passaged virus interfered with the multiplication of the standard JHM virus, but not with vesicular stomatitis virus. After sucrose equilibrium centrifugation of high passage virus, a single peak contained both infectious virus and interfering activity. This virus population resembled the original JHM virus in its structural proteins, but it contained an increased proportion of a protein with a molecular weight of 65 X 10(3). Genomic RNA from standard JHM virus contained a single species of RNA with a molecular weight of 5.4 X 10(6). After five undiluted passages, however, the virion population contained two RNA species with molecular weights of 5.4 X 10(6) and 5.2 X 10(6). RNase T1 resistant oligonucleotide finger-printing of these RNAs showed that the lower molecular weight RNA had lost several oligonucleotide spots that were present in the genomic RNA of the standard JHM virus. After several serial diluted passages of passage 10 virus, a single virus population was obtained which again had only standard virus RNA with a molecular weight of 5.4 X 10(6) and lacked interfering activity. These results indicated that defective interfering particles were generated by serial undiluted passages of JHM virus.

Animals↗