Enterocin CRL35 inhibits late stages of HSV-1 and HSV-2 replication in vitro
The replication of herpes simplex virus (HSV) type 1 and 2 in Vero cells is inhibited in the presence of enterocin CRL35 (ECRL), a bacteriocin produced by Enterococcus faecium CRL35. Attempts to resolve the mode of action of ECRL indicate that virus adsorption and penetration are not affected. Inste...
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2003
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01663542_v58_n1_p17_Wachsman http://hdl.handle.net/20.500.12110/paper_01663542_v58_n1_p17_Wachsman |
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paper:paper_01663542_v58_n1_p17_Wachsman2023-06-08T15:15:40Z Enterocin CRL35 inhibits late stages of HSV-1 and HSV-2 replication in vitro Antiviral Bacteriocin Enterococcus faecium Herpes simplex type 1 and 2 bacteriocin enterocin crl35 glycoprotein D late gamma protein monoclonal antibody unclassified drug virus antigen virus protein animal cell antigen expression antiviral activity article cell fusion cell size concentration response controlled study drug activity drug effect Enterococcus faecium herpes Herpes simplex virus 1 Herpes simplex virus 2 nonhuman priority journal protein expression protein synthesis inhibition Vero cell virus adsorption virus inhibition virus mutant virus replication Enterococcus Enterococcus faecium Human herpesvirus 1 Human herpesvirus 2 Simplexvirus The replication of herpes simplex virus (HSV) type 1 and 2 in Vero cells is inhibited in the presence of enterocin CRL35 (ECRL), a bacteriocin produced by Enterococcus faecium CRL35. Attempts to resolve the mode of action of ECRL indicate that virus adsorption and penetration are not affected. Instead, a late step of virus multiplication is hindered since the addition of 100μg/ml of ECRL at 8h post infection still causes a 90% inhibition of virus release. The effect of ECRL on HSV antigen expression was studied by immunofluorescence using a polyclonal serum and a monoclonal antibody against glycoprotein D (γ protein). These studies indicated that ECRL impeded the second round of infection, apparently as a consequence of the inhibition of glycoprotein D expression. The replication of syncytial mutants of HSV-1 was significantly inhibited at a ECRL concentration of 25μg/ml. Both the percentage of fused cells and the polykaryocyte size were affected. Studies on the effect of ECRL on viral protein synthesis showed that in the presence of ECRL, HSV late γ proteins were not synthesized. From these findings, it is concluded that inhibition of HSV spreading by ECRL is due to the prevention of mainly late glycoprotein synthesis. © 2003 Elsevier Science B.V. All rights reserved. 2003 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01663542_v58_n1_p17_Wachsman http://hdl.handle.net/20.500.12110/paper_01663542_v58_n1_p17_Wachsman |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
Antiviral Bacteriocin Enterococcus faecium Herpes simplex type 1 and 2 bacteriocin enterocin crl35 glycoprotein D late gamma protein monoclonal antibody unclassified drug virus antigen virus protein animal cell antigen expression antiviral activity article cell fusion cell size concentration response controlled study drug activity drug effect Enterococcus faecium herpes Herpes simplex virus 1 Herpes simplex virus 2 nonhuman priority journal protein expression protein synthesis inhibition Vero cell virus adsorption virus inhibition virus mutant virus replication Enterococcus Enterococcus faecium Human herpesvirus 1 Human herpesvirus 2 Simplexvirus |
| spellingShingle |
Antiviral Bacteriocin Enterococcus faecium Herpes simplex type 1 and 2 bacteriocin enterocin crl35 glycoprotein D late gamma protein monoclonal antibody unclassified drug virus antigen virus protein animal cell antigen expression antiviral activity article cell fusion cell size concentration response controlled study drug activity drug effect Enterococcus faecium herpes Herpes simplex virus 1 Herpes simplex virus 2 nonhuman priority journal protein expression protein synthesis inhibition Vero cell virus adsorption virus inhibition virus mutant virus replication Enterococcus Enterococcus faecium Human herpesvirus 1 Human herpesvirus 2 Simplexvirus Enterocin CRL35 inhibits late stages of HSV-1 and HSV-2 replication in vitro |
| topic_facet |
Antiviral Bacteriocin Enterococcus faecium Herpes simplex type 1 and 2 bacteriocin enterocin crl35 glycoprotein D late gamma protein monoclonal antibody unclassified drug virus antigen virus protein animal cell antigen expression antiviral activity article cell fusion cell size concentration response controlled study drug activity drug effect Enterococcus faecium herpes Herpes simplex virus 1 Herpes simplex virus 2 nonhuman priority journal protein expression protein synthesis inhibition Vero cell virus adsorption virus inhibition virus mutant virus replication Enterococcus Enterococcus faecium Human herpesvirus 1 Human herpesvirus 2 Simplexvirus |
| description |
The replication of herpes simplex virus (HSV) type 1 and 2 in Vero cells is inhibited in the presence of enterocin CRL35 (ECRL), a bacteriocin produced by Enterococcus faecium CRL35. Attempts to resolve the mode of action of ECRL indicate that virus adsorption and penetration are not affected. Instead, a late step of virus multiplication is hindered since the addition of 100μg/ml of ECRL at 8h post infection still causes a 90% inhibition of virus release. The effect of ECRL on HSV antigen expression was studied by immunofluorescence using a polyclonal serum and a monoclonal antibody against glycoprotein D (γ protein). These studies indicated that ECRL impeded the second round of infection, apparently as a consequence of the inhibition of glycoprotein D expression. The replication of syncytial mutants of HSV-1 was significantly inhibited at a ECRL concentration of 25μg/ml. Both the percentage of fused cells and the polykaryocyte size were affected. Studies on the effect of ECRL on viral protein synthesis showed that in the presence of ECRL, HSV late γ proteins were not synthesized. From these findings, it is concluded that inhibition of HSV spreading by ECRL is due to the prevention of mainly late glycoprotein synthesis. © 2003 Elsevier Science B.V. All rights reserved. |
| title |
Enterocin CRL35 inhibits late stages of HSV-1 and HSV-2 replication in vitro |
| title_short |
Enterocin CRL35 inhibits late stages of HSV-1 and HSV-2 replication in vitro |
| title_full |
Enterocin CRL35 inhibits late stages of HSV-1 and HSV-2 replication in vitro |
| title_fullStr |
Enterocin CRL35 inhibits late stages of HSV-1 and HSV-2 replication in vitro |
| title_full_unstemmed |
Enterocin CRL35 inhibits late stages of HSV-1 and HSV-2 replication in vitro |
| title_sort |
enterocin crl35 inhibits late stages of hsv-1 and hsv-2 replication in vitro |
| publishDate |
2003 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01663542_v58_n1_p17_Wachsman http://hdl.handle.net/20.500.12110/paper_01663542_v58_n1_p17_Wachsman |
| _version_ |
1768544681630629888 |