Association of deoxyribonuclease-sensitive material with adenovirus penton aggregates after treatment of infected cell cultures with sodium deoxycholate

1971 ◽  
Vol 17 (8) ◽  
pp. 1009-1013 ◽  
Author(s):  
R. G. Marusyk ◽  
E. Norrby
Keyword(s):  
Infected Cell ◽  
Cell Cultures ◽  
Buoyant Density ◽  
Sodium Deoxycholate ◽  
High Density ◽  
Monomeric Form ◽  
Sensitive Material ◽  
Dna Labeling ◽  
Infected Cells ◽  
Simian Adenovirus

Sodium deoxycholate treatment of adenovirus-infected cell cultures was found to release rapidly sedimenting penton components with a buoyant density in CsCl of about 1.34 g/ml. The high-density penton material derived from human and simian adenovirus-infected cells occurred in monomeric form, while that derived from canine adenovirus-infected cells was in the form of non-symmetrical groupings of pentons aggregated at the vertex capsomere. Deoxyribonuclease treatment and 3H-thymidine-DNA labeling experiments revealed that the high-density of the pentons so obtained was due to a small associated segment of nuclease-sensitive material. A possible explanation of the nature of the nuclease-sensitive material is given.

Isolation and preliminary characterization of herpes Channel Catfish virus DNA

1980 ◽  
Vol 26 (2) ◽  
pp. 130-134 ◽  
Author(s):  
Jean Robin ◽  
Alice Rodrigue
Keyword(s):  
Channel Catfish ◽  
Gradient Centrifugation ◽  
Buoyant Density ◽  
Sedimentation Coefficient ◽  
Sodium Deoxycholate ◽  
Cesium Chloride ◽  
Equilibrium Density ◽  
Channel Catfish Virus ◽  
Phenol Extraction ◽  
Infected Cells

The DNA of Channel Catfish virus (CCV) was selectively extracted from infected cells with a 5% solution of sodium deoxycholate, deproteinized using sodium sarcosinate and pronase, and purified by phenol extraction followed by equilibrium density gradient centrifugation in a cesium chloride solution. CCV DNA displays a buoyant density of 1.715 g/cm3 in such a solution, as would be expected from a duplex DNA containing 56.1% of guanine plus cytosine. As estimated from both its sedimentation coefficient and length in the electron microscope, CCV DNA is a linear duplex molecule of approximately 85 × 106 daltons.

scholarly journals LEUKOTACTIC FACTORS ELABORATED BY VIRUS-INFECTED TISSUES

1972 ◽  
Vol 135 (5) ◽  
pp. 1095-1103 ◽  
Author(s):  
Peter A. Ward ◽  
Stanley Cohen ◽  
Thomas D. Flanagan
Keyword(s):  
Infected Cell ◽  
Cell Cultures ◽  
Allantoic Fluid ◽  
Protective Role ◽  
Cell System ◽  
Mumps Virus ◽  
Chemotactic Activity ◽  
Mammalian Cell Cultures ◽  
Infected Cells

Infection of chick embryos wih either Newcastle disease virus or mumps virus and infection of BGM cell cultures with mumps virus result in the elaboration of chemotactic activity for neutrophils and macrophages. These factors cannot be found in lysates of uninfected cells. They do not appear to be associated with the viral particles per se, but rather are present in virus-free supernates from infected fluids. Ultracentrifugal studies of the neutrophil chemotactic activity in allantoic fluid of embryos infected with the two different viruses indicate a similar biphasic distribution of activity, while fluid from the mammalian cell cultures shows a single zone of leukotactic activity, further suggesting that the infected cell, rather than the virus, is responsible for the leukotactic activity. Virus-infected cells also release a substance(s) which is itself not leukotactic but which can interact with human C3 or C5 to generate such activity. This leukotactic factor-generating substance is similar to that reported in another virus-infected cell system. It is postulated that the leukotactic factors elaborated as a result of virus infection of cells may play a protective role in vivo.

scholarly journals Sequence Variability of Borna Disease Virus: Resistance to Superinfection May Contribute to High Genome Stability in Persistently Infected Cells

2000 ◽  
Vol 74 (17) ◽  
pp. 7878-7883 ◽  
Author(s):  
Stephan Formella ◽  
Christian Jehle ◽  
Christian Sauder ◽  
Peter Staeheli ◽  
Martin Schwemmle
Keyword(s):  
Infected Cell ◽  
Disease Virus ◽  
Cell Cultures ◽  
Wild Type Virus ◽  
Type Virus ◽  
Wild Type ◽  
Borna Disease Virus ◽  
Persistently Infected ◽  
Infected Cells ◽  
Borna Disease

ABSTRACT The RNA genome of Borna disease virus (BDV) shows extraordinary stability in persistently infected cell cultures. We performed bottleneck experiments in which virus populations from single infected cells were allowed to spread through cultures of uninfected cells and in which RNase protection assays were used to identify virus variants with mutations in a 535-nucleotide fragment of the M-G open reading frames. In one of the cell cultures, the major virus species (designated 2/1) was a variant with two point mutations in the G open reading frame. When fresh cells were infected with a low dose of a virus stock prepared from 2/1-containing cells, only a minority of the resulting persistently infected cultures contained detectable levels of the variant, whereas the others all seemed to contain wild-type virus. The BDV variant 2/1 remained stable in the various persistently infected cell cultures, indicating that the cells were resistant to superinfection by wild-type virus. Indeed, cells persistently infected with prototype BDV He/80 were also found to resist superinfection with strain V and vice versa. Our screen for mutations in the viral M and G genes of different rat-derived BDV virus stocks revealed that only one of four stocks believed to contain He/80 harbored virus with the original sequence. Two stocks mainly contained a novel virus variant with about 3% sequence divergence, whereas the fourth stock contained a mixture of both viruses. When the mixture was inoculated into the brains of newborn mice, the novel variant was preferentially amplified. These results provide evidence that the BDV genome is mutating more frequently than estimated from its invariant appearance in persistently infected cell cultures and that resistance to superinfection might strongly select against novel variants.

Further Observations on the Virus of Epizootic Diarrhea of Infant Mice. An Electron Microscopic Study

1967 ◽  
Vol 25 ◽  
pp. 110-111
Author(s):  
W. G. Banfield ◽  
G. Kasnic ◽  
J. H. Blackwell
Keyword(s):  
Electron Microscope ◽  
Infected Cell ◽  
Microscopic Study ◽  
Intestinal Epithelium ◽  
Ultrastructural Study ◽  
Osmium Tetroxide ◽  
Lead Citrate ◽  
Electron Microscopic ◽  
Virus Particles ◽  
Infected Cells

An ultrastructural study of the intestinal epithelium of mice infected with the agent of epizootic diarrhea of infant mice (EDIM virus) was first performed by Adams and Kraft. We have extended their observations and have found developmental forms of the virus and associated structures not reported by them.Three-day-old NLM strain mice were infected with EDIM virus and killed 48 to 168 hours later. Specimens of bowel were fixed in glutaraldehyde, post fixed in osmium tetroxide and embedded in epon. Sections were stained with uranyl magnesium acetate followed by lead citrate and examined in an updated RCA EMU-3F electron microscope.The cells containing virus particles (infected) are at the tips of the villi and occur throughout the intestine from duodenum through colon. All developmental forms of the virus are present from 48 to 168 hours after infection. Figure 1 is of cells without virus particles and figure 2 is of an infected cell. The nucleus and cytoplasm of the infected cells appear clearer than the cells without virus particles.

scholarly journals Remodeling the Endoplasmic Reticulum by Poliovirus Infection and by Individual Viral Proteins: an Autophagy-Like Origin for Virus-Induced Vesicles

2000 ◽  
Vol 74 (19) ◽  
pp. 8953-8965 ◽  
Author(s):  
David A. Suhy ◽  
Thomas H. Giddings ◽  
Karla Kirkegaard
Keyword(s):  
Endoplasmic Reticulum ◽  
Mammalian Cells ◽  
Buoyant Density ◽  
Rna Replication ◽  
Viral Proteins ◽  
Replication Complex ◽  
Poliovirus Infection ◽  
Endosomal Membranes ◽  
Infected Cells ◽  
Positive Strand Rna

ABSTRACT All positive-strand RNA viruses of eukaryotes studied assemble RNA replication complexes on the surfaces of cytoplasmic membranes. Infection of mammalian cells with poliovirus and other picornaviruses results in the accumulation of dramatically rearranged and vesiculated membranes. Poliovirus-induced membranes did not cofractionate with endoplasmic reticulum (ER), lysosomes, mitochondria, or the majority of Golgi-derived or endosomal membranes in buoyant density gradients, although changes in ionic strength affected ER and virus-induced vesicles, but not other cellular organelles, similarly. When expressed in isolation, two viral proteins of the poliovirus RNA replication complex, 3A and 2C, cofractionated with ER membranes. However, in cells that expressed 2BC, a proteolytic precursor of the 2B and 2C proteins, membranes identical in buoyant density to those observed during poliovirus infection were formed. When coexpressed with 2BC, viral protein 3A was quantitatively incorporated into these fractions, and the membranes formed were ultrastructurally similar to those in poliovirus-infected cells. These data argue that poliovirus-induced vesicles derive from the ER by the action of viral proteins 2BC and 3A by a mechanism that excludes resident host proteins. The double-membraned morphology, cytosolic content, and apparent ER origin of poliovirus-induced membranes are all consistent with an autophagic origin for these membranes.

Cytochemistry of the wall of infected cells in Casuarina actinorhizae

1988 ◽  
Vol 66 (10) ◽  
pp. 2038-2047 ◽  
Author(s):  
R. Howard Berg ◽  
Lorraine McDowell
Keyword(s):  
Infected Cell ◽  
Secondary Wall ◽  
Chromic Acid ◽  
Cortical Cell ◽  
Wall Material ◽  
Primary Cell Wall ◽  
Acid Digestion ◽  
En Bloc ◽  
Lignin Modification ◽  
Infected Cells

Development of the wall of infected cells in Casuarina actinorhizae differs from that of many actinorhizae. After the endophyte penetrates the wall of a cortical cell, that (primary) cell wall becomes lignified, based on histochemical (autofluorescence, phloroglucinol staining) and cytochemical (permanganate staining, enzyme etching) evidence. Subsequently, the remaining walls of the infected cell become lignified. Adjacent noninfected cells somehow are stimulated to deposit a lignified secondary wall only on those walls bordering the infected cell. This remarkable participation of all adjacent noninfected cells in the development of a given infected cell results in an increased thickness and strength of the wall material surrounding infected cells. When they mature, there is a further modification of some of the wall layers surrounding infected cells, manifested in a relative impermeability to en bloc staining with permanganate. Unlike lignified walls, the permanganate-impermeable region is selectively stained by osmium or ferricyanide-reduced osmium and is relatively resistant to concentrated chromic acid digestion. A region that remains permeable to (and stained by) permanganate (part of the secondary wall of bordering noninfected cells) may be developmentally related to phi thickenings. An earlier contention that the permanganate-impermeable region contains suberin is unconfirmed. This region is most likely an unusual lignin modification or results from unidentified material impregnated in its ligninlike matrix.

An RNA polymerase II transcription factor inactivated in poliovirus-infected cells copurifies with transcription factor TFIID

1988 ◽  
Vol 8 (8) ◽  
pp. 3175-3182
Author(s):  
S Kliewer ◽  
A Dasgupta
Keyword(s):  
Transcription Factor ◽  
Infected Cell ◽  
Rna Polymerase ◽  
Host Cell ◽  
Rna Polymerase Ii ◽  
Heat Inactivation ◽  
Early Event ◽  
Cell Extracts ◽  
Infected Cells ◽  
Rna Polymerase Ii Transcription

Inhibition of host cell RNA polymerase II-mediated transcription by poliovirus infection was studied in vitro. Whole-cell extracts prepared from poliovirus-infected HeLa cells at 3 h postinfection were shown to be deficient in a factor required for specific transcription from the adenovirus major late promoter. Three lines of evidence suggest that transcription factor TFIID is deficient in poliovirus-infected cells. First, the activity required to specifically restore transcription in poliovirus-infected cell extracts was shown to copurify with TFIID through three chromatographic steps. Second, transcription reactions reconstituted with phosphocellulose-derived chromatographic fractions revealed a fourfold decrease in the specific activity of the TFIID-containing fraction prepared from poliovirus-infected cells compared with that of the same fraction prepared from mock-infected cells. Finally, TFIID and the activity required to specifically restore transcription in virus-infected cell extracts were shown to have the same kinetics of heat inactivation. Together, these results suggest that inactivation of TFIID is an early event in the inhibition of host cell RNA polymerase II transcription by poliovirus.

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