PubMed Health⌕ Search

Biomedical subjects

S B Bond

Publications and source records attributed to S B Bond.

7 recordsLinked to original sources
PubMed1984

Infection of human vascular endothelial cells by Rickettsia rickettsii.

Rocky Mountain spotted fever is caused by Rickettsia rickettsii, an obligate intracellular bacterial parasite. The organism primarily attacks endothelial cells and occasionally attacks smooth-muscle cells of small blood vessels. An effective means of examining host-parasite interaction in Rocky Mountain spotted fever would be to use an in vitro model system with a host-cell type that is similar in structure and function to the putative target cell in human infections. Because human umbilical-vein endothelial cells in culture retain many, if not all, of their characteristic properties in vivo and because they also share many properties of capillary endothelium, the use of this endothelial cell system is appropriate in the study of the interaction between R rickettsii and the cell that is principally parasitized in humans. Uptake by umbilical-vein endothelial-cell cultures of R rickettsii is dose dependent. The organism replicates in both the nucleus and cytoplasm of infected cells and exhibits early cell-to-cell spread without detectable host-cell injury.

Cells, Cultured↗
PubMed1978

Polyoma virus-human cell interactions: persistence of T-antigen in two cell lines with and without transformation.

The interaction of polyoma virus and human cells was investigated. Abortive infection as evidenced by the synthesis of T-antigen was observed in normal fibroblast and abnormal (transformed) cells but not in normal epithelial cells. A high percentage of simian virus 40-transformed WI-18 Va2 and spontaneously transformed BE skin cells produced T-antigen after high-multiplicity infection, but most of the cells rapidly lost antigen-producing capacity upon cell passage, and the cultures became negative by passage 3. All fibroblast cells displayed varying degrees of susceptibility to infection, but most of the cell lines became negative for T-antigen except for two. In one, T-antigen persisted in a small percentage of the cells throughout the lifetime of the culture, without cellular transformation occurring. In the other, the entire culture became morphologically transformed and eventually consisted of 100% T-antigen-positive cells. This is the first time that normal diploid human fibroblast cells have been transformed by polyoma virus.

Animals↗
PubMed1978

Characterization of K virus and its comparison with polyoma virus.

The antigenic relationship between the two murine papovaviruses, K virus and polyoma virus, was examined by serological techniques to determine whether they shared any antigenic components. No cross-reactivity was found associated with the viral (V) antigens by the indirect immunofluorescence, neutralization, or hemagglutination-inhibition tests. The tumor (T) antigens expressed in transformed cells or cells productively infected by either K or polyoma virus did not cross-react by indirect immunofluorescence. An antigenic relationship was detected, however, among the late proteins of K virus, polyoma virus, simian virus 40, and the human papovavirus BKV, when tested with either hyperimmune sera prepared against polyoma virus and simian virus 40 or sera prepared against disrupted virions. The nucleic acids of K and polyoma viruses were compared by agarose gel electrophoresis and restriction endonuclease analysis. No nucleotide sequence homology between the genomes of these two viruses was detectable by DNA-DNA hybridization techniques under stringent conditions. The genome of K virus was found to be slightly smaller than that of polyoma virus, and the cleavage patterns of the viral DNAs with six restriction endonucleases were different. These findings indicate that there is little relationship between these two murine papovaviruses.

Antigens, Viral↗