Endocytosis of simian virus 40 into the endoplasmic reticulum.

Abstract

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.

Misfolded major histocompatibility complex class I molecules accumulate in an expanded ER-Golgi intermediate compartment.

“…A post-ER, pre-Golgi compartment was identified as a differentiated proximal portion of the intermediate compartment (Hobman et al, 1992) and the complex tubular network accumulating class I HCs and 132m's described in the present study is morphologically similar. A region of anastomosing tubular membranes in continuity with the RER, similar to the compartments referred to above, was also described as the site of accumulation of endocytosed Simian virus 40 (Kartenbeck et al, 1989). Our observations extend the findings on virus or viral glycoproteins to other multimeric proteins such as class I molecules, and do so in primary cells in situ.…”

“…5). The morphology of the class I-enriched reticulum, as observed in plastic-embedded and positively contrasted material, is reminiscent of the site of assembly and accumulation of virus or unassembled viral glycoproteins observed in the CV1 and CHO cell lines (Kartenbeck et al, 1989;Hobman et al, 1992). An antibody that recognizes four ER membrane proteins and is known to label post-ER derivatives (Louvard et al, 1982;Noda and Farquar, 1992), stains the dense tubules and the vesiculated areas enriched in class I HCs (Fig.…”

BK Polyoma Virus Allograft Nephropathy: Ultrastructural Features from Viral Cell Entry to Lysis

“…These organelles, called caveosomes, start fusing with each other and undergo rapid shape changes, including formation of long tubular structures (10). These tubules have no attached ribosomes, but they are in continuity with the rough endoplasmic reticulum (32). The extensive network of tubules and vesicles that transport the virions from one part of the cell to another is also consistent with recently described cisternal compartments within intracellular transport pathways that include branching tubular elements that can be several micrometers long (33).…”

Extracellular Simian Virus 40 Induces an ERK/MAP Kinase-independent Signalling Pathway that Activates Primary Response Genes and Promotes Virus Entry

“…The likelihood that SV40 infectious entry is promoted by a signal transmitted from the cell surface is interesting with respect to the following: firstly, whereas most viruses that enter cells by endocytosis enter in clathrin-coated vesicles (Marsh & Helenius, 1989), SV40 enters cells in non-coated vesicles (Maul et al, 1978;Kartenbeck et al, 1989). These noncoated vesicles might at this time be referred to as caveolae (e.g.…”