Mengovirus-induced Capping of Virus Receptors on the Plasma Membrane of Ehrlich Ascites Tumour Cells

SUMMARYThe infection of animal cells by encephalomyocarditis (EMC) virus lead to a drastic change in membrane permeability towards low tool. wt. compounds. Addition of the nucleotide analogue GppCH2P to the culture medium resulted in a specific inhibition of protein synthesis in EMC virus-infected 3T6 cells. This inhibition was not observed when GTP or ATP were present nor in control mock-infected 3T6 cells. The induction of membrane leakiness after viral infection was not specific for 3T6 cells, as it was also detected in mouse L cells, hamster BHK-21 cells and monkey CV1 cells. The inhibitory action produced by GppCH2p in virus-infected cells was fully reversed upon addition of fresh medium. Moreover, analysis of the proteins synthesized after medium replacement showed a preferential synthesis of cellular proteins. The presence of zinc ions resulted in an inhibition of the cleavage of large viral polypeptide precursors to mature viral proteins. Under these conditions, membrane leakiness as measured by GppCH2p, was not observed. However, this seems to be an effect of zinc ions themselves on the membrane, because inhibition of mature protein fOrmation by other means, such as the presence of amino acid analogues, did not prevent inhibition of translation by GppCH2P in virus-infected cells.Addition of the cap analogues 7mGppp and 2'-O'-mGppp, resulted in specific stimulation of viral protein synthesis in EMC virus-infected 3T6 cells. On the other hand, the presence of 7mGp had no effect on translation. We propose that a specific capping of viral mRNA takes place in the presence of these compounds, and leads to increased stability and greater efficiency in the translation of viral mRNA.

Section: Effect Of Cap Analogues On Protein Synthesis In Emc Virus-insupporting

confidence: 56%

Action of Nucleotide Derivatives on Translation in Encephalomyocarditis Virus-infected Mouse Cells

Carrasco

1981

“…However, attachment of the virus particle to the appropriate receptor molecules in the host cell plasma membrane is considered to be the initial step in all virus infections. Recent results from several viruses suggest that, after attachment, virus particles may be redistributed over the cell surface (Gschwender & Traub, 1979;Helenius et aL, 1980;Patterson & Macnaughton, 1981;Alstiel & Landsberger, 1981) by a mechanism that is temperature-and energy-dependent (Patterson & Macnaughton, 1981). Migration on the cell surface may or may not be an important prerequisite for virus internalization.…”

Section: Introductionmentioning

confidence: 99%

Ultrastructural and Immunofluorescence Studies of Early Events in Adenovirus-HeLa Cell Interactions

Patterson¹,

Russell²

1983

SUMMARYScanning electron microscopy and immunofluorescence techniques show that the attachment of adenovirus type 5 to HeLa cells is followed by a temperature-dependent redistribution of virus particles on the cell surface. Metabolic inhibitors and cytochalasin B, a drug that impairs microfilament function, blocked this redistribution. Transmission electron microscopy studies demonstrated that inhibition of redistribution was paralleled by an inhibition of virus internalization. In further experiments virus and cells were incubated at 4 °C and then treated with adenovirus 'soluble' antigens to block unoccupied virus receptors. On warming these preparations to37 °C, the internalization of attached virions was found to be impaired. It is proposed that energy-dependent redistribution of attached adenovirus particles on the cell surface facilitates entry by bringing virions into contact with sufficient receptors to allow internalization.

“…Such binding may result in a redistribution of virus particles on the cell surface by mechanisms similar to those operating in antibody-or lectin-mediated capping. Recent investigations with a picornavirus suggest that such a redistribution can occur (Gschwender & Traub, 1979).…”

Section: Introductionmentioning

confidence: 99%

The Distribution of Human Coronavirus Strain 229E on the Surface of Human Diploid Cells

Patterson

Macnaughton

1981

SUMMARYThe distribution of human coronavirus strain 229E (HCV 229E) particles on the surface of human diploid (MRCc) cells was examined. Virus particles showed a totally random distribution on fixed cells and on cells to which virus had been adsorbed in the cold. A marked redistribution of virus particles was observed on warming virus-cell preparations to 33 °C for 20 rain, the peripheral areas of the cell becoming relatively devoid of virus particles while the majority of particles were now located some distance from the edge of the cell. Redistribution did not occur in the presence of metabolic inhibitors.