Enveloped viruses as model membrane systems: microviscosity of vesicular stomatitis virus and host cell membranes

Biochemistry ◽  
1976 ◽  
Vol 15 (16) ◽  
pp. 3563-3570 ◽  
Author(s):  
Yechezkel Barenholz ◽  
Norman F. Moore ◽  
Robert R. Wagner
2014 ◽  
Vol 17 (5) ◽  
pp. 607-620 ◽  
Author(s):  
Jens Jäger ◽  
Susanne Keese ◽  
Manfred Roessle ◽  
Michael Steinert ◽  
Andra B. Schromm

2021 ◽  
Vol 120 (3) ◽  
pp. 321a
Author(s):  
Rui Su ◽  
Jin Zeng ◽  
Sathish Thiyagarajan ◽  
Ben O'Shaughnessy

1985 ◽  
Vol 101 (1) ◽  
pp. 60-65 ◽  
Author(s):  
M Ono ◽  
K Mifune ◽  
A Yoshimura ◽  
S Ohnishi ◽  
M Kuwano

A mutant (MO-5) resistant to monensin (an ionophoric antibiotic) derived from the mouse Balb/3T3 cell line, was a poor host for vesicular stomatitis virus (VSV) or semliki forest virus (SFV) multiplication. The yield of VSV particles in MO-5 is one 100-fold reduced as is VSV-dependent RNA synthesis. In contrast to a pH-remedial mutant, the abortive production of infectious VSV particles in MO-5 cells was not restored by low pH treatment. The pH values in the endosome and the lysosome of MO-5 cells were 5.2 and 5.4, respectively, values that were comparable to the pH value in Balb/3T3 cells. Assays with [3H]uridine-labeled VSV indicated similar binding of VSV in MO-5: percoll gradient centrifugation analysis of [35S]methionine-labeled VSV-infected Balb/3T3 showed accumulation of VSV in the lysosome fraction 20 min after VSV infection, whereas VSV can be found mainly in endosome/Golgi fraction of MO-5 cells after 40 to 60 min on the percoll gradients. Degradation of [35S]methionine-labeled VSV was observed at a significant rate in Balb/3T3 cells, but not in MO-5 cells. The monensin-resistant somatic cell may thus provide a genetic route to study the mechanism of endocytosis or transport of enveloped viruses.


2004 ◽  
Vol 49 (3) ◽  
pp. 685-704 ◽  
Author(s):  
Leigh A. Knodler ◽  
Bruce A. Vallance ◽  
Michael Hensel ◽  
Daniela Jäckel ◽  
B. Brett Finlay ◽  
...  

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