Next Article in Journal
Inhibition Profiling of Retroviral Protease Inhibitors Using an HIV-2 Modular System
Previous Article in Journal
Silencing of a Germin-Like Protein Gene (CchGLP) in Geminivirus-Resistant Pepper (Capsicum chinense Jacq.) BG-3821 Increases Susceptibility to Single and Mixed Infections by Geminiviruses PHYVV and PepGMV
Article Menu

Export Article

Open AccessArticle
Viruses 2015, 7(12), 6108-6126; doi:10.3390/v7122928

Activation of the Mitochondrial Apoptotic Signaling Platform during Rubella Virus Infection

1
Institute of Virology, University of Leipzig, 04103 Leipzig, Germany
2
Division of Clinical Pharmacology, Ludwig-Maximilian University Munich, 80336 Munich, Germany
3
WHO European Regional Reference Laboratory for Measles and Rubella, Robert Koch-Institute, 13353 Berlin, Germany
4
Department of Biology, Georgia State University, Atlanta, GA 30303, USA
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Academic Editor: Curt Hagedorn
Received: 3 August 2015 / Revised: 16 November 2015 / Accepted: 17 November 2015 / Published: 26 November 2015
(This article belongs to the Section Antivirals & Vaccines)
View Full-Text   |   Download PDF [2610 KB, uploaded 31 December 2015]   |  

Abstract

Mitochondria- as well as p53-based signaling pathways are central for the execution of the intrinsic apoptotic cascade. Their contribution to rubella virus (RV)-induced apoptosis was addressed through time-specific evaluation of characteristic parameters such as permeabilization of the mitochondrial membrane and subsequent release of the pro-apoptotic proteins apoptosis-inducing factor (AIF) and cytochrome c from mitochondria. Additionally, expression and localization pattern of p53 and selected members of the multifunctional and stress-inducible cyclophilin family were examined. The application of pifithrin μ as an inhibitor of p53 shuttling to mitochondria reduced RV-induced cell death to an extent similar to that of the broad spectrum caspase inhibitor z-VAD-fmk (benzyloxycarbonyl-V-A-D-(OMe)-fmk). However, RV progeny generation was not altered. This indicates that, despite an increased survival rate of its cellular host, induction of apoptosis neither supports nor restricts RV replication. Moreover, some of the examined apoptotic markers were affected in a strain-specific manner and differed between the cell culture-adapted strains: Therien and the HPV77 vaccine on the one hand, and a clinical isolate on the other. In summary, the results presented indicate that the transcription-independent mitochondrial p53 program contributes to RV-induced apoptosis. View Full-Text
Keywords: mPTP; p53; AIF; cyclophilin family; CypA; Cyp40; cytochrome c; NIM811; PFTμ mPTP; p53; AIF; cyclophilin family; CypA; Cyp40; cytochrome c; NIM811; PFTμ
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Claus, C.; Manssen, L.; Hübner, D.; Roßmark, S.; Bothe, V.; Petzold, A.; Große, C.; Reins, M.; Mankertz, A.; Frey, T.K.; Liebert, U.G. Activation of the Mitochondrial Apoptotic Signaling Platform during Rubella Virus Infection. Viruses 2015, 7, 6108-6126.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Viruses EISSN 1999-4915 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top