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Published on: February 22, 2017
Increased mitochondrial functions in human glioblastoma cells persistently infected with measles virus
Megumi Takahashi1, Alexander M Wolf, Eiji Watari
1Department of Microbiology and Immunology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan.
Abstract:
Measles virus (MV) is known for its ability to cause an acute infection with a potential of development of persistent infection. However, knowledge of how viral genes and cellular factors interact to cause or maintain the persistent infection has remained unclear. We have previously reported the possible involvement of mitochondrial short chain enoyl-CoA hydratase (ECHS), which is localized at mitochondria, in the regulation of MV replication. In this study we found increased functions of mitochondria in MV-persistently infected cells compared with uninfected or acutely infected cells. Furthermore, impairment of mitochondrial functions by treatment with mitochondrial inhibitors such as ethidium bromide (EtBr) or carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP) induced the cytopathic effects of extensive syncytial formation in persistently infected cells. These findings suggest that mitochondria are one of the subcellular organelles contributing to regulate persistent infection of MV. Recent studies showed mitochondria provide an integral platform for retinoic acid-inducible protein (RIG-I)-like cytosolic receptors (RLRs) signaling and participate in cellular innate antiviral immunity. Our findings not only reveal a role of mitochondria in RLR mediated antiviral signaling but also suggest that mitochondria contribute to the regulation of persistent viral infection.
Insights
Mitochondria play a key role in regulating persistent measles virus (MV) infection. Impairing mitochondrial function in infected cells triggers severe cytopathic effects, highlighting their importance in viral persistence.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- Measles virus (MV) can establish persistent infections, but the underlying mechanisms involving host-pathogen interactions remain poorly understood.
- Mitochondrial short chain enoyl-CoA hydratase (ECHS) has been previously implicated in regulating MV replication.
- The precise role of mitochondria in the maintenance of persistent viral infections is an area requiring further investigation.
Purpose of the Study:
- To investigate the role of mitochondria in regulating persistent measles virus (MV) infection.
- To determine how mitochondrial function is altered in MV-persistently infected cells.
- To explore the consequences of impairing mitochondrial function on MV persistence and cellular pathology.
Main Methods:
- Comparative analysis of mitochondrial function in uninfected, acutely infected, and persistently infected cells.
- Treatment of persistently infected cells with mitochondrial inhibitors (e.g., ethidium bromide, FCCP).
- Assessment of cytopathic effects, including syncytial formation, in response to mitochondrial dysfunction.
Main Results:
- Mitochondrial functions were significantly increased in MV-persistently infected cells compared to controls.
- Impairment of mitochondrial function using inhibitors induced extensive syncytial formation in persistently infected cells.
- These results indicate that mitochondria are crucial for regulating persistent MV infection.
Conclusions:
- Mitochondria are subcellular organelles that contribute significantly to the regulation of persistent measles virus infection.
- Mitochondria are involved in retinoic acid-inducible protein (RIG-I)-like receptor (RLR) mediated antiviral signaling.
- The study underscores a novel role for mitochondria in both innate antiviral immunity and the persistence of viral infections.
