A new plaque system for canine distemper: characteristics of the green strain of canine distemper virus

1979 ◽  
Vol 25 (6) ◽  
pp. 680-685 ◽  
Author(s):  
C. K. Ho ◽  
L. A. Babiuk
Keyword(s):  
Canine Distemper Virus ◽  
Cell Types ◽  
Kidney Cells ◽  
Canine Distemper ◽  
Kinetics Of Adsorption ◽  
Green Strain ◽  
Dog Kidney ◽  
Infected Cells ◽  
Kinetics Of ◽  
Cellular Destruction

A Vero cell adapted Green strain of canine distemper virus (CDV) was tested for its plaque-forming capacity in different cell lines. Plaque formation was observed in HEp-2, BS-C-I, and HeLa cells but not in Vero or dog kidney cells even though replication and cytopathology were observed in the latter cell types. In the cells in which the virus was capable of producing plaques, the plaques were observed within 24 h post infection and continued to increase in size with subsequent cellular destruction such that by 72 h postinfection the size of the plaques approached 0.5 mm. With the use of the plaquing technique, it was possible to demonstrate the thermal lability of the virus as well as the kinetics of adsorption. Thus, it was shown that the half-life of the virus was 125 min at 25 °C, 75 min at 35 °C, and 65 min at 37 °C. The rate of adsorption of CDV to HEp-2 cells was 17.2% in 30 min at 37 °C and continued slowly for 4 h before completion. Application of this rapid plaque-forming assay to plaque-reduction tests for CDV antibody and for CDV-infected cells by the infectious center assay are described.

scholarly journals Virulent and attenuated canine distemper virus infects multiple dog brain cell types in vitro

Glia ◽  
1991 ◽  
Vol 4 (4) ◽  
pp. 408-416 ◽  
Author(s):  
Susan Pearce-Kelling ◽  
William J. Mitchell ◽  
Brian A. Summers ◽  
Max J. G. Appel
Keyword(s):  
Canine Distemper Virus ◽  
Cell Types ◽  
Brain Cell ◽  
Canine Distemper ◽  
Dog Brain ◽  
Brain Cell Types

Mannose 6-phosphate receptor-dependent endocytosis of lysosomal enzymes is increased in sulfatide-storing kidney cells

2009 ◽  
Vol 390 (1) ◽  
Author(s):  
Diana Klein ◽  
Afshin Yaghootfam ◽  
Ullrich Matzner ◽  
Bettina Koch ◽  
Thomas Braulke ◽  
...  
Keyword(s):  
Lysosomal Enzymes ◽  
Cell Types ◽  
Recycling Rate ◽  
Kidney Cells ◽  
Lysosomal Disorder ◽  
Renal Tubular Cells ◽  
Internalization Rate ◽  
Mannose 6 Phosphate ◽  
Renal Tubular ◽  
Kinetics Of

Abstract Metachromatic leukodystrophy is a lysosomal disorder caused by the deficiency of arylsulfatase A (ASA). This leads to the storage of the sphingolipid 3-O-sulfogalactosylceramide (sulfatide) in various cell types, such as renal tubular cells. Examination of mannose 6-phosphate receptor (MPR300)-dependent endocytosis revealed that uptake of lysosomal enzymes is more than two-fold increased in sulfatide-storing kidney cells. Expression of MPR300 and its internalization rate is increased in these cells, whereas the recycling rate is decreased. Similar alterations can be found for the transferrin receptor, indicating that sulfatide storage leads to a general alteration of the endocytotic pathway. These data allow calculating that the endosomal pool from which receptors can recycle is 1.4- to 2-fold increased in lipid-storing cells. Immunocytochemistry demonstrates that the MPR300 in lipid-storing cells does not co-localize with accumulated sulfatide, suggesting that the kinetics of internalization and recycling appear to be altered indirectly.

scholarly journals Dual infection with an emergent strain of canine distemper virus and canine parvovirus in an Arctic wolf under managed care

2019 ◽  
Vol 31 (4) ◽  
pp. 594-597 ◽  
Author(s):  
Justin M. Stilwell ◽  
Eman Anis ◽  
Rebecca P. Wilkes ◽  
Daniel R. Rissi
Keyword(s):  
Canine Distemper Virus ◽  
Wild Type Strain ◽  
Cell Types ◽  
Dual Infection ◽  
Acute Onset ◽  
Canine Parvovirus ◽  
Long Bones ◽  
Canine Distemper ◽  
Conventional Pcr ◽  
Intracytoplasmic Inclusions

A 6-wk-old managed male Arctic wolf with lethargy, drooling, dehydration, elevated temperature, and acute onset of seizures was submitted for autopsy. The wolf had been vaccinated with a multivalent vaccine exactly 2 wk prior to presentation. Grossly, long bones were brittle and easily fractured under pressure; the intestinal contents were mucoid and yellow. Histologically, there was widespread lymphoid and hematopoietic necrosis, failure of endochondral ossification within long bones, as well as intranuclear and intracytoplasmic inclusions in various tissues and cell types. Canine distemper virus was detected in numerous tissues by IHC and confirmed by RT-rtPCR and sequencing as an American-4 strain, an emerging strain in domestic dogs and wildlife species in the southeastern United States. The clinical and pathologic findings associated with this emergent CDV strain have not been reported previously in wolves, to our knowledge. Canine parvovirus 2 (CPV-2b) was also detected in the spleen by IHC and confirmed by conventional PCR as a wild-type strain. The exact impact of CPV-2b on the clinical course is unknown. Early vaccination in this case may have predisposed this Artic wolf to developing clinical disease.

scholarly journals Cell Fusion by Canine Distemper Virus-Infected Cells

1972 ◽  
Vol 10 (6) ◽  
pp. 1179-1183 ◽  
Author(s):  
Anne M. Rankin ◽  
Linda E. Fisher ◽  
Robert H. Bussell
Keyword(s):  
Cell Fusion ◽  
Canine Distemper Virus ◽  
Canine Distemper ◽  
Infected Cells

Electron Autoradiography of Adenovlrus Infected Cells

1970 ◽  
Vol 28 ◽  
pp. 168-169 ◽  
Author(s):  
T. Yamamoto ◽  
M.S. Shahrabadi
Keyword(s):  
Kidney Cells ◽  
Specific Enzyme ◽  
Morphological Alterations ◽  
Spherical Inclusions ◽  
Dog Kidney ◽  
Large Virus ◽  
Infected Cells ◽  
Dark Staining ◽  
Light Staining ◽  
And Function

The sequential morphological alterations in dog kidney cells infected with a canine adenovirus has previously been shown (3) to produce several intranuclear inclusions: (a) early DNA containing inclusions which form ringshaped structures and rapidly expand to form a large virus synthesizing mass; (b) dark staining spherical inclusions; (c) light staining inclusions: and (d) the virus aggregates which at later times, form crystals (Fig. 1). This report is an analysis of the nature and function of these inclusions with respect to the replicating virus using specific enzyme digestion and autoradiographic techniques.

scholarly journals Specialization for cell-free or cell-to-cell spread of BAC-cloned HCMV strains is determined by factors beyond the UL128-131 and RL13 loci

2019 ◽  
Author(s):  
Eric P. Schultz ◽  
Jean-Marc Lanchy ◽  
Le Zhang Day ◽  
Qin Yu ◽  
Christopher Peterson ◽  
...  
Keyword(s):  
Neutralizing Antibodies ◽  
Early Time ◽  
Cell Types ◽  
Conceptual Approach ◽  
Bac Clone ◽  
Intact Cells ◽  
A Cell ◽  
Infected Cells ◽  
Kinetics Of ◽  
Cell Spread

ABSTRACTIt is widely held that clinical isolates of human cytomegalovirus (HCMV) are highly cell-associated, and mutations affecting the UL128-131 and RL13 loci that arise in culture lead to the appearance of a cell-free spread phenotype. The BAC-clone Merlin (ME), expresses abundant UL128-131, is RL13-impaired and produces low infectivity virions in fibroblasts, whereas TB40/e (TB) and TR are low in UL128-131, RL13-intact and produce virions of much higher infectivity. Despite these differences, quantification of spread by flow cytometry revealed remarkably similar spread efficiencies in fibroblasts. In epithelial cells, ME spread more efficiently, consistent with robust UL128-131 expression. Strikingly, ME spread far better than TB or TR in the presence of neutralizing antibodies on both cell types, indicating that ME is not simply deficient at cell-free spread, but is particularly efficient at cell-to-cell spread, whereas TB and TR cell-to-cell spread is poor. Sonically disrupted ME-infected cells contained scant infectivity, suggesting that the efficient cell-to-cell spread mechanism of ME depends on features of the intact cells such as junctions or intracellular trafficking processes. Even when UL128-131 was transcriptional repressed, cell-to-cell spread of ME was still more efficient than TB or TR. Moreover, RL13 expression comparably reduced both cell-free and cell-to-cell spread of all three strains, suggesting that it acts at a stage of assembly and/or egress common to both routes of spread. Thus, HCMV strains can be highly specialized for either for cell-free or cell-to-cell spread and these phenotypes are determined by factors beyond the UL128-131 or RL13 loci.IMPORTANCEBoth cell-free and cell-to-cell spread are likely important for the natural biology of HCMV. In culture, strains clearly differ in their capacity for cell-free spread as a result of differences in the quantity and infectivity of extracellular released progeny. However, it has been unclear whether “cell-associated” phenotypes are simply the result of poor cell-free spread, or are indicative of particularly efficient cell-to-cell spread mechanisms. By measuring the kinetics of spread at early time points, we were able to show that HCMV strains can be highly specialized to either cell-free or cell-to-cell mechanisms, and this was not strictly linked the efficiency of cell-free spread. Our results provide a conceptual approach to evaluating intervention strategies for their ability to limit cell-free or cell-to-cell spread as independent processes.

scholarly journals Canine Distemper Virus Selectively Inhibits Apoptosis Progression in Infected Immune Cells

2009 ◽  
Vol 83 (12) ◽  
pp. 6279-6287 ◽  
Author(s):  
Stéphane Pillet ◽  
Veronika von Messling
Keyword(s):  
Cell Cycle ◽  
Immune Cells ◽  
Canine Distemper Virus ◽  
Mononuclear Cells ◽  
Mdck Cells ◽  
Clinical Signs ◽  
Epithelial Cell Line ◽  
Canine Distemper ◽  
Peripheral Blood Mononuclear ◽  
Infected Cells

ABSTRACT Morbillivirus infections are characterized by severe leukopenia and immune suppression that develop even before the onset of clinical signs. To characterize in more detail the fate of the immune cells during the critical first week, we evaluated the overall viability, level of apoptosis, cell cycle status, and extent of infection in different immune tissues of ferrets inoculated with a lethal canine distemper virus (CDV) strain. Initial experiments with MDCK cells, a canine epithelial cell line, revealed that CDV infection resulted in only a marginal increase in apoptosis at high infection levels and that infected cells were more resistant to chemically induced apoptosis. In ferrets, levels of viability and early and late apoptosis remained stable in thymus and lymph node, where more than 80% of cells were infected, whereas a gradual albeit small increase in apoptosis was observed in peripheral blood mononuclear cells and spleen. Furthermore, the progression of spontaneous apoptosis in infected cells was inhibited, while the proportion of apoptotic noninfected “bystander” cells increased. The distribution of cells in the different stages of the cell cycle in the bone marrow was not affected, but dividing cells in the thymus decreased by 50%, and a 10-fold increase in cell division was noted in the spleen. It is unlikely that the extent of infection-induced cell death and cell cycle alterations alone can account for the dramatic leukopenia observed in this model. The investigation of additional mechanisms is therefore warranted.

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