Cell sonicates used in the analysis of how measles and herpes simplex type 1 virus infections influence Vero cell mitochondrial calcium uptake

1985 ◽  
Vol 63 (11) ◽  
pp. 1194-1197 ◽  
Author(s):  
Karen Lund ◽  
Barry Ziola

Brief sonication was used to rapidly prepare an in situ mitochondrial Ca2+ uptake system from Vero cells. This method yielded intact, functional mitochondria capable of accumulating and retaining approximately 50% of Ca2+ available in the reaction mix. Mitochondria in cells infected with herpes simplex type 1 virus exhibited a gradual decline in the initial Ca2+ uptake rate, dropping to 65% of the control rate at the end of the 12-h lytic cycle. Influence of a lytic measles virus infection on the initial Ca2+ upake rate was different. The rate initially dropped to 75% of the control rate by 9 h postinfection, then recovered to slightly above the control rate at 21 h postinfection, and finally declined to 75% of the control rate at 30 h postinfection. Neither viral infection altered the total amount of Ca2+ accumulated by Vero cell mitochondria.

1983 ◽  
Vol 3 (4) ◽  
pp. 712-719
Author(s):  
E Bedows ◽  
K M Rao ◽  
M J Welsh

In herpes simplex virus type 1-infected Vero cells, reorganization of microfilaments was observed approximately 4 h postinfection. Conversion of F (filamentous) actin to G (globular) actin, as assessed by a DNase I inhibition assay, was continuous over the next 12 to 16 h, at which time a level of G actin of about twice that observed in uninfected cells was measured. Fluorescent localization of F actin, using 7-nitrobenz-2-oxa-1,3-diazole (NBD)-phallacidin, demonstrated that microfilament fibers began to diminish at about 16 to 18 h postinfection, roughly corresponding to the time that G actin levels peaked and virus-induced cytopathology was first observable. In measles virus-infected cells, no such disassembly of microfilaments occurred. Rather, there was a modest decrease in G actin levels. Fluorescent localization of F actin showed that measles virus-infected Vero cells maintained a complex microfilament network characterized by fibers which spanned the entire length of the newly formed giant cells. Disruption of microfilaments with cytochalasin B, which inhibits measles virus-specific cytopathology, was not inhibitory to measles virus production at high multiplicities of infection (MOI) but was progressively inhibitory as the MOI was lowered. The carbobenzoxy tripeptide SV-4814, which inhibits the ability of Vero cells to fuse after measles virus infection, like cytochalasin B, inhibited measles virus production at low MOI but not at high MOI. Thus, it appears that agents which affect the ability of Vero cells to fuse after measles virus infection may be inhibitory to virus production and that the actin network is essential to this process.


1983 ◽  
Vol 3 (4) ◽  
pp. 712-719 ◽  
Author(s):  
E Bedows ◽  
K M Rao ◽  
M J Welsh

In herpes simplex virus type 1-infected Vero cells, reorganization of microfilaments was observed approximately 4 h postinfection. Conversion of F (filamentous) actin to G (globular) actin, as assessed by a DNase I inhibition assay, was continuous over the next 12 to 16 h, at which time a level of G actin of about twice that observed in uninfected cells was measured. Fluorescent localization of F actin, using 7-nitrobenz-2-oxa-1,3-diazole (NBD)-phallacidin, demonstrated that microfilament fibers began to diminish at about 16 to 18 h postinfection, roughly corresponding to the time that G actin levels peaked and virus-induced cytopathology was first observable. In measles virus-infected cells, no such disassembly of microfilaments occurred. Rather, there was a modest decrease in G actin levels. Fluorescent localization of F actin showed that measles virus-infected Vero cells maintained a complex microfilament network characterized by fibers which spanned the entire length of the newly formed giant cells. Disruption of microfilaments with cytochalasin B, which inhibits measles virus-specific cytopathology, was not inhibitory to measles virus production at high multiplicities of infection (MOI) but was progressively inhibitory as the MOI was lowered. The carbobenzoxy tripeptide SV-4814, which inhibits the ability of Vero cells to fuse after measles virus infection, like cytochalasin B, inhibited measles virus production at low MOI but not at high MOI. Thus, it appears that agents which affect the ability of Vero cells to fuse after measles virus infection may be inhibitory to virus production and that the actin network is essential to this process.


1981 ◽  
Vol 67 (4) ◽  
pp. 333-339 ◽  
Author(s):  
T. Gotlieb-Stematsky ◽  
J. Zonis ◽  
A. Arlazoroff ◽  
T. Mozes ◽  
M. Sigal ◽  
...  

Author(s):  
Rosângela Maria Callou Pinheiro ◽  
Maria Tereza Villela Romanos ◽  
Antonio Canabarro ◽  
Ana Cecília Aranha ◽  
Maíra Prado ◽  
...  

1985 ◽  
Vol 6 (11) ◽  
pp. 456-458 ◽  
Author(s):  
Robert Z. Cavagnolo

AbstractThe adequacy of a currently recommended protocol for disinfecting CPR manikins was investigated. Known quantities of Herpes simplex type 1 virus were applied to various sites on both adult and infant manikin heads, exposed to disinfectant under simulated classroom conditions, and then assayed for infectious virus. Results indicate that the disinfecting protocol and disinfectant are adequate for inactivating herpesvirus on CPR manikins, but that care must be exercised to ensure thorough cleaning.


2008 ◽  
Vol 14 (2) ◽  
pp. 102-118 ◽  
Author(s):  
Biborka Bereczky-Veress ◽  
Olle Lidman ◽  
Farideh Sabri ◽  
Ivan Bednar ◽  
Fredrik Granath ◽  
...  

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