Electron microscopic examination of cytoplasmic inclusion bodies in cells infected with parainfluenza virus, type 2

Virology ◽  
1963 ◽  
Vol 21 (3) ◽  
pp. 527-530 ◽  
Author(s):  
N.O. Kuhn ◽  
C.G. Harford
2006 ◽  
Vol 54 (1) ◽  
pp. 51-60 ◽  
Author(s):  
Míra Mándoki ◽  
M. Dobos-Kovács ◽  
T. Bakonyi ◽  
M. Rusvai

Kidney samples from chickens diagnosed with acute nephritis and gout were subjected to histological and electron microscopic examination. The investigations revealed cytoplasmic inclusion bodies in the tubular epithelial cells containing round virions of about 30 nm in diameter. Since avian nephritis virus (ANV) is known as a potential causative agent of the so-called baby chick nephropathy, an RT-PCR assay was developed for the molecular detection of ANV-specific nucleic acid in the specimen. The specificity of the assay was confirmed by direct sequencing of the amplicon obtained in the reaction. The nucleotide sequence of the PCR product showed 92% identity with the reference ANV sequence deposited in the GenBank database. After having been validated on some other suspicious cases of avian nephritis, the PCR method described in this study can be a potential tool for routine diagnostic examination of samples submitted from cases of gout and nephropathy in chickens.


Virology ◽  
1967 ◽  
Vol 31 (1) ◽  
pp. 92-100 ◽  
Author(s):  
Masanori Tajima ◽  
Takeshi Ushijima ◽  
Shigeru Kishi ◽  
Junji Nakamura

1978 ◽  
Vol 29 (6) ◽  
pp. 1235 ◽  
Author(s):  
RS Greber

Watermelon mosaic virus type 1 (WMV-1) has not previously been reported from Australia and has become prevalent in Queensland only since 1970. Watermelon mosaic virus type 2 (WMV-2) continues to reach a high incidence in marrow (Cucurbita pepo) and pumpkin (Cucurbita maxima and Cucurbita moschata) crops, WMV-2 is rarely isolated from watermelons (Citrullus vulgaris) in which epidemics of WMV-1 now cause serious reductions in yield. The Queensland Blue cultivar of C. maxima, the most important cucurbit crop, produces severely distorted fruit following infection by WMV-1, although it is little affected by WMV-2. Physical properties of these WMV isolates and electron microscopic examination of the virus particles and associated cellular inclusions showed them to be similar to those reported elsewhere, but there were some distinctive host reactions for the WMV-2 isolates. No resistance to either WMV-1 or WMV-2 was found in commercially available C. pepo, C. maxima or C. vulgaris. The resistance of Cucumis metuliferus to Australian WMV-1 isolates was confirmed, and a source of resistance to both WMV-1 and WMV-2 was found in Lagenaria siceravia. Methods of separation of WMV-1 and WMV-2 from mixed isolates and methods for the identification of each on differential hosts and by serology were shown to be effective.


Author(s):  
W.T. Gunning ◽  
A.F. Gohara ◽  
T.E. Walsh ◽  
E.P. Calomeni

A thirty-six year old male with severe congestive heart failure was given a cardiac transplant. The findings of the evaluation of his native heart is the basis for this presentation. Our findings included the identification of unusual cytoplasmic inclusion bodies found throughout the heart. These inclusions, found most often in a perinuclear location, were eosinophilic and crystalloid at the light microscopic level (Figure 1.). Special histologic stains were not supportive of a diagnosis of nemaline rod disease as a trichrome stain failed to differentiate inclusions from surrounding cytoplasm, yet could be accomplished with PAS staining (Figure 2.) . Furthermore, the ultrastructural morphology of the inclusions did not show any similarity to z-band material, the electron microscopic characteristic of inclusion bodies in nemaline rod myopathy. The shape of these bodies was usually rectangular or elliptical (Figure 3.) and size was found to be quite variable, some measured in excess of 15μ X 4μ. Other characteristics included an amorphous appearance with occasional electron densities within the inclusions (Figure 3), an apparent single limiting membrane (Figure 3 and 4), and for some of the inclusions, there was a suggestion of secondary lysosomal association (Figure 4).


2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Vincent Rincheval ◽  
Mickael Lelek ◽  
Elyanne Gault ◽  
Camille Bouillier ◽  
Delphine Sitterlin ◽  
...  

2005 ◽  
Vol 79 (22) ◽  
pp. 14112-14121 ◽  
Author(s):  
T. S. Carlos ◽  
R. Fearns ◽  
R. E. Randall

ABSTRACT Although parainfluenza virus 5 (simian virus 5 [SV5]) circumvents the interferon (IFN) response by blocking IFN signaling and by reducing the amount of IFN released by infected cells, its ability to circumvent the IFN response is not absolute. The effects of IFN on SV5 infection were examined in Vero cells, which do not produce but can respond to IFN, using a strain of SV5 (CPI−) which does not block IFN signaling. Thus, by infecting Vero cells with CPI− and subsequently treating the cells with exogenous IFN, it was possible to observe the effects that IFN had on SV5 infection in the absence of virus countermeasures. IFN rapidly (within 6 h) induced alterations in the relative levels of virus mRNA and protein synthesis and caused a redistribution of virus proteins within infected cells that led to the enhanced formation of virus cytoplasmic inclusion bodies. IFN induced a steeper gradient of mRNA transcription from the 3′ to the 5′ end of the genome and the production of virus mRNAs with longer poly(A) tails, suggesting that the processivity of the virus polymerase was altered in cells in an IFN-induced antiviral state. Additional evidence is presented which suggests that these findings also apply to the replication of strains of SV5, parainfluenza virus type 2, and mumps virus that block IFN signaling when they infect cells that are already in an IFN-induced antiviral state.


1979 ◽  
Vol 16 (1) ◽  
pp. 6-17 ◽  
Author(s):  
S. D. Kosanke ◽  
K. R. Pierce ◽  
W. K. Read

The neurons and glial cells of 1- to 140-day-old pigs with GM2-gangliosidosis had membranous cytoplasmic inclusion bodies. These bodies appeared as small vacuolated cytoplasmic structures in paraffin-embedded, hematoxylin and eosin-stained sections and as solid, dark, round granules in 1-micrometer sections embedded in plastic and stained with toluidine blue. Ultrastructurally, the cytoplasmic inclusion bodies appeared as round, dense structures from 0.6 to 1.2 micrometers in diameter, that were filled with various amounts of small to large arrays of membranous lamellae. The cortical neuronal inclusions were seen initially as lysosomes containing a small amount of particulate material. The appearance of these inclusions changed as they progressed through different configurational stages. Inclusions resembled the granulomembranous body, the zebra body, possibly other intermediate forms and, finally, the classical membranous cytoplasmic body. The cytoplasmic inclusions in glial cells resembled membranovesicular bodies and, although also of apparent lysosomal origin, were morphologically different from the neuronal inclusions. The morphologic lesions in the neurons and glial cells of the affected pigs were similar to those described for human gangliosidoses.


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