Morphological Aspects of the Uptake of Simian Virus 40 by Permissive Cells

Hummeler, Klaus; Tomassini, N; Sokol, F.

doi:10.1128/jvi.6.1.87-93.1970

Cited by 107 publications

(43 citation statements)

References 18 publications

(14 reference statements)

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“…Other viruses have means for transporting their genomes into the nucleus, without relying on the host cell's progression through mitosis. SV40 (Hummeler et al, 1970;Clever et al, 1991) and influenza virus (Martin and Helenius, 1991) particles can apparently migrate through the nuclear pore. Electron micrographs suggest that other viruses, including adenovirus (Dales and Chardonnet, 1973), granulosis virus (Summers, 1971) and herpes simplex virus (Miyamoto and Morgan, 1971;Tognon et al, 1981;Batterson et al, 1983) bind their viral cores to the nuclear pore to transfer their DNA into the nucleus.…”

Section: Discussionmentioning

confidence: 99%

Integration of murine leukemia virus DNA depends on mitosis.

et al. 1993

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In synchronized rat or mouse cells infected with Moloney murine leukemia virus (MLV), integration of viral DNA and production of viral proteins occur only after the cells traverse mitosis. Integration is blocked when cells are prevented from progressing through mitosis. Viral nucleoprotein complexes isolated from arrested cells contain full‐length viral DNA and can integrate this viral DNA in vitro, showing that the block to integration in arrested cells is not due to a lack of mature integration machinery. When infected cells traverse mitosis, there is a sharp increase in nuclear accumulation of viral DNA. The dependence of integration on mitosis may therefore be due to a requirement for mitosis and nuclear envelope breakdown for entry of the viral integration complex into the nucleus.

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Section: Discussionmentioning

confidence: 99%

Integration of murine leukemia virus DNA depends on mitosis.

et al. 1993

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“…Early studies on SV40 entry found the internalisation pathway to differ in several ways from the classical clathrinmediated endocytic process described for many viruses. Firstly, electron micrographs of SV40-infected cells showed the majority of particles in small tight-fitting vesicles, which appeared to be uncoated (Hummeler et al 1970). These vesicles were able to fuse to generate larger compartments within the cell (which we now term caveosomes; Maul et al 1978).…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of viral entry: sneaking in the front door

2010

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Recent developments in methods to study virus internalisation are providing clearer insights into mechanisms used by viruses to enter host cells. The use of dominant negative constructs, specific inhibitory drugs and RNAi to selectively prevent entry through particular pathways has provided evidence for the clathrin-mediated entry of hepatitis C virus (HCV) as well as the caveolar entry of Simian Virus 40. Moreover, the ability to image and track fluorescent-labelled virus particles in real-time has begun to challenge the classical plasma membrane entry mechanisms described for poliovirus and human immunodeficiency virus. This review will cover both well-documented entry mechanisms as well as more recent discoveries in the entry pathways of enveloped and non-enveloped viruses. This will include viruses which enter the cytosol directly at the plasma membrane and those which enter via endocytosis and traversal of internal membrane barrier(s). Recent developments in imaging and inhibition of entry pathways have provided insights into the ill-defined entry mechanism of HCV, bringing it to the forefront of viral entry research. Finally, as high-affinity receptors often define viral internalisation pathways, and tropism in vivo, host membrane proteins to which viral particles specifically bind will be discussed throughout.

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“…Morphological studies of SV-40 and polyoma virus entry have suggested, however, that all viruses may not be as disciplined in their interactions with cellular organelles. These nonenveloped viruses, which belong to the papovavirus family, have been seen to enter the cells via small tight-fitting, uncoated membrane vesicles ("monopinocytotic" vesicles) derived from the plasma membrane (13,15,19,23,24). Incoming virus particles have also been reported in a variety of cellular compartments, including the nucleoplasm, the lysosomes, the ER, and mitochondria (15,19,23,24).…”

mentioning

confidence: 99%

Endocytosis of simian virus 40 into the endoplasmic reticulum.

Kartenbeck

Stukenbrok

Helenius

1989

The Journal of Cell Biology

239

241

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Abstract. The endocytosis of SV-40 into CV-1 cells was studied using biochemical and ultrastructural techniques. The half-time of binding of [35S]methionineradiolabeled SV-40 to CV-1 cells was 25 min. Most of the incoming virus particles remained undegraded for several hours. Electron microscopy showed that some virus entered the endosomal/lysosomal pathway via coated vesicles, while the majority were endocytosed via small uncoated vesicles. After infection at high multiplicity, one third of total cell-associated virus was observed to enter the ER, starting 1-2 h after virus application. The viruses were present in large, tubular, smooth membrane networks generated as extentions of the ER. The results describe a novel and unique membrane transport pathway that allows endocytosed viral particles to be targeted from the plasma membrane to the ER.

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Morphological Aspects of the Uptake of Simian Virus 40 by Permissive Cells

Cited by 107 publications

References 18 publications

Integration of murine leukemia virus DNA depends on mitosis.

Integration of murine leukemia virus DNA depends on mitosis.

Mechanisms of viral entry: sneaking in the front door

Endocytosis of simian virus 40 into the endoplasmic reticulum.

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