PubMed Health⌕ Search

Biomedical subjects

V Stollar

Publications and source records attributed to V Stollar.

At least 73 records · Page 4Linked to original sources
PubMed1978

Immunofluorescent detection of nuclear double-stranded RNA in situ in Vero and mosquito cells.

Double-stranded RNA (dsRNA) was detected in situ by indirect immunofluorescence with antibodies to dsRNA. It was seen in nuclei of Vero and Aedes albopictus cells, but not in BHK cells, KB cells, chick embryo fibroblasts, or HeLa cells. Reactive dsRNA was present in the nucleoplasm, but not in nucleoli or cytoplasm. Extracted RNA from the whole cell contained from 0.08 percent (BHK) to 0.46 percent (HeLa) dsRNA, as estimated by serological methods. This dsRNA, found in molecules having the size distribution of heterogeneous nuclear RNA, did not renature rapidly after denaturation. The quantity of dsRNA in total extracted RNA did not correlate with the presence or absence of nuclear staining in situ.

Cell Line↗
PubMed1978

Isolation and partial characterization of drug-resistant Aedes albopictus cells.

We report here the first isolation and characterization of drug-resistant cell lines from cultured mosquito cells. A BrdU-resistant cell line was isolated from mutagen-treated Aedes albopictus cells, and then used as the parent cell from which sublines resistant to ouabain or alpha-amanitin were derived. The BrdU-resistant cell line and all sublines derived from it were shown to be deficient in thymidine kinase. Evidence that favored attributing the drug-resistant phenotypes to mutant genotypes included (a) the drug-resistant phenotypes were stable for up to 16 months of culture under nonselective conditions, and (b) the frequency of the ouabain-resistant cells in a sensitive population was increased 500-fold (to between 10(-3) and 10(-4) by exposure to the chemical mutagen EMS. Evidence illustrating the usefulness of mutant mosquito cells for the study of the genetics of somatic cells is discussed.

Aedes↗
PubMed1977

The significance and nature of defective interfering viruses.

Deletions in viral genomes appear to be a common occurrence in the replication of all DNA and RNA viruses which have been adequately studied. Such defective genomes can replicate in the presence in the same cell of a helper virus as long as the deletion does not involve the initiation site for genome replication. Coinfection of a cell with defective and "normal" infectious virus leads to reduction in the yield of the latter. The nature of DI viruses and genomes found in Sindbis virus-infected vertebrate cells during "undiluted passage" series is discussed. This procedure leads to the accumulation of progressively shorter viral RNA genomes with internal deletions. The enrichment is limited to genome lengths which are integral fractions (1/2, 1/3, 1/4, etc.) of the complete genome, and these are also found in viral particles released at the corresponding passage levels. It is believed that the selective accumulation of these fragments is governed by constraints of assembly which demand that one full genome equivalent be packaged in a released particle. In contrast to vertebrate cells, cultured mosquito cells do not seem to produce or "recognize" DI particles. Possible implications for the epidemiology of arthropod-transmitted alphaviruses are presented.

Animals↗
PubMed1976

Failure of defective interfering particles of Sindbis virus produced in BHK or chicken cells to affect viral replication in Aedes albopictus cells.

Whereas defective interfering particles of Sindbis virus are readily produced in BHK-21 cells or chicken embryo fibroblasts by the techniques of serial undiluted passage, similar methods failed to generate such particles in Aedes albopictus cell cultures. In addition, Sindbis virus stocks produced in BHK-21 cells or chicken embryo fibroblasts and which contained defective interfering particles, when tested in A. albopictus cells, failed (i) to interfere with the replication of standard Sindbis virus and (ii) to change the pattern of intracellular viral RNA synthesis from that produced by infection with standard Sindbis virus alone. We conclude that defective interfering particles of Sindbis virus generated in chicken or hamster cells are silent or inert in mosquito cells.

Adsorption↗