Electron microscopic studies on frog virus 3 infection in HeLa cells at permissive and non-permissive temperatures

1974 ◽  
Vol 45 (4) ◽  
pp. 376-381 ◽  
Author(s):  
Ester Zylber-Katz ◽  
A. Lazar ◽  
Pnina Weisman
Author(s):  
J. Heppell ◽  
L. Berthiaume

Fish lymphocystis disease is a common viral infection reported in over a hundred teleost species. The causative agent, Lymphocystis disease virus (LDV), has been classified in the Iridoviridae family. Though it has an icosahedral shape, its capsid is complex and still not very well characterized. However, several studies have been reported on the ultrastructure of Frog virus 3 (FV3), another iridovirus, showing outside protein units with an underlying lipidic layer, surrounding the viral core. In order to verify whether or not the structure of LDV particles correspond to that of FV3 , a comparative electron microscopic study was undertaken.LDV strain Leetown (ATCC VR-342) was propagated on BF-2 cells, and FV3 strain Granoff (ATCC VR-567) on FHM cells. Viral particles, concentrated and suspended in 0.1M Tris buffer (pH appropriate for the enzyme used), were adsorbed on formvar-coated grids prior to digestion with proteases (pronase E or proteinase K, 20 U/ml) and/or phospholipases (A2 or C, 15 U/ml) at 37°C for various incubation periods. Particles were negatively stained with 2% (w/v) phosphotungstic acid pH 6.0 before examination with a Philips 300 transmission electron microscope (TEM) at 80 kV.


1974 ◽  
Vol 25 (3) ◽  
pp. 405-413 ◽  
Author(s):  
E. Zylber-Katz ◽  
P. Weisman

1998 ◽  
Vol 4 (S2) ◽  
pp. 1028-1029
Author(s):  
J. R. Palisano ◽  
J. L. Thacker ◽  
C. S. Piromalli ◽  
A. M. Morrison ◽  
J. E. Tate

The origin and role of confronting cisternae (CC) have been clouded in mystery since their discovery in 1955. Early investigations suggested that CC arose from either nuclear envelope (NE) or by stacking of endoplasmic reticulum (ER) cisternae. Electron microscopic studies of mitotic HeLa cells suggest that CC are fragments of NE (Fig. 1) that arise as portions of the NE fold back on one another. Because lamin B is a NE specific protein, a monoclonal antibody to lamin B was used to probe the origin of CC. The monoclonal antibody to lamin B was then detected by utilizing a secondary antibody conjugated to the fluorochrome rhodamine which fluoresces red when exposed to UV light. Fluorescent microscopy of interphase HeLa cells demonstrates that only the NE fluoresces red when the cells are probed with a monoclonal antibody to lamin B (Fig. 2). There is no label localized in the cytoplasm which supports the evidence that lamin B is only localized to the NE in interphase cells.


Virology ◽  
1974 ◽  
Vol 58 (2) ◽  
pp. 589-594 ◽  
Author(s):  
G.E. Houts ◽  
M. Gravell ◽  
Allan Granoff

Author(s):  
Jan Zarzycki ◽  
Joseph Szroeder

The mammary gland ultrastructure in various functional states is the object of our investigations. The material prepared for electron microscopic examination by the conventional chemical methods has several limitations, the most important are the protein denaturation processes and the loss of large amounts of chemical constituents from the cells. In relevance to this,one can't be sure about a degree the observed images are adequate to the realy ultrastructure of a living cell. To avoid the disadvantages of the chemical preparation methods,some autors worked out alternative physical methods based on tissue freezing / freeze-drying, freeze-substitution, freeze-eatching techniqs/; actually the technique of cryoultraraicrotomy,i,e.cutting ultrathin sections from deep frozen specimens is assented as a complete alternative method. According to the limitations of the routine plastic embbeding methods we were interested to analize the mammary gland ultrastructure during lactation by the cryoultramicrotomy method.


Author(s):  
F. G. Zaki ◽  
E. Detzi ◽  
C. H. Keysser

This study represents the first in a series of investigations carried out to elucidate the mechanism(s) of early hepatocellular damage induced by drugs and other related compounds. During screening tests of CNS-active compounds in rats, it has been found that daily oral administration of one of these compounds at a dose level of 40 mg. per kg. of body weight induced diffuse massive hepatic necrosis within 7 weeks in Charles River Sprague Dawley rats of both sexes. Partial hepatectomy enhanced the development of this peculiar type of necrosis (3 weeks instead of 7) while treatment with phenobarbital prior to the administration of the drug delayed the appearance of necrosis but did not reduce its severity.Electron microscopic studies revealed that early development of this liver injury (2 days after the administration of the drug) appeared in the form of small dark osmiophilic vesicles located around the bile canaliculi of all hepatocytes (Fig. 1). These structures differed from the regular microbodies or the pericanalicular multivesicular bodies. They first appeared regularly rounded with electron dense matrix bound with a single membrane. After one week on the drug, these vesicles appeared vacuolated and resembled autophagosomes which soon developed whorls of concentric lamellae or cisterns characteristic of lysosomes (Fig. 2). These lysosomes were found, later on, scattered all over the hepatocytes.


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