ArticleJournal of virology2008
Theiler's virus-induced intrinsic apoptosis in M1-D macrophages is Bax mediated and restricts virus infectivity: a mechanism for persistence of a cytolytic virus.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Critical role of TLR activation in viral replication, persistence, and pathogenicity of Theiler's virus.Frontiers in immunology · 2023Review
- Excessive Innate Immunity Steers Pathogenic Adaptive Immunity in the Development of Theiler's Virus-Induced Demyelinating Disease.International journal of molecular sciences · 2021Review
- During Infection, Theiler's Virions Are Cleaved by Caspases and Disassembled into Pentamers.Journal of virology · 2016Article
- Inhibition of Theiler's virus-induced apoptosis in infected murine macrophages results in necroptosis.Virus research · 2015Article
- Saffold virus is able to productively infect primate and rodent cell lines and induces apoptosis in these cells.Emerging microbes & infections · 2014Article
- Mutation of the Theiler's virus leader protein zinc-finger domain impairs apoptotic activity in murine macrophages.Virus research · 2013Article
- Modeling the acute and chronic phases of Theiler murine encephalomyelitis virus infection.Journal of virology · 2013Article
- The antiapoptotic protein Mcl-1 controls the type of cell death in Theiler's virus-infected BHK-21 cells.Journal of virology · 2012Article
- Apoptotic and antiapoptotic activity of L protein of Theiler's murine encephalomyelitis virus.Journal of virology · 2011Article
- The proapoptotic Bcl-2 protein Bax plays an important role in the pathogenesis of reovirus encephalitis.Journal of virology · 2011Article
- Virus susceptibility of Chinese hamster ovary (CHO) cells and detection of viral contaminations by adventitious agent testing.Biotechnology and bioengineering · 2010Article
- Cytokine/chemokine profile in J774 macrophage cells persistently infected with DA strain of Theiler's murine encephalomyelitis virus (TMEV).Journal of neurovirology · 2010Article
- Theiler's murine encephalomyelitis virus L* amino acid position 93 is important for virus persistence and virus-induced demyelination.Journal of virology · 2010Article
- Interactions between viral and prokaryotic pathogens in a mixed infection with cardiovirus and mycoplasma.Journal of virology · 2009Article
- Activation of tumor suppressor protein p53 is required for Theiler's murine encephalomyelitis virus-induced apoptosis in M1-D macrophages.Journal of virology · 2009Article
- Theiler's murine encephalomyelitis virus leader protein is the only nonstructural protein tested that induces apoptosis when transfected into mammalian cells.Journal of virology · 2009Article
- Th17 cells enhance viral persistence and inhibit T cell cytotoxicity in a model of chronic virus infection.The Journal of experimental medicine · 2009Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Theiler's murine encephalomyelitis virus (TMEV), a member of the Cardiovirus genus in the family Picornaviridae, is a highly cytolytic virus that produces necrotic death in rodent cells except for macrophages, which undergo apoptosis. In the present study we have analyzed the kinetics of BeAn virus infection in M1-D cells, in order to temporally relate virus replication to the apoptotic signaling events. Apoptosis was associated with early exponential virus growth from 1 to 12 h postinfection (p.i.); however, >/=80% of peak infectivity was lost by 16 to 24 h p.i. The pan-caspase inhibitor qVD-OPh led to significantly higher virus yields, while zVAD-fmk completely inhibited virus replication until 10 h p.i., precluding its assessment in apoptosis. In contrast, while zVAD-fmk significantly inhibited BeAn virus replication in BHK-21 cells at 12 and 16 h p.i., virus replication at these time points was not altered by qVD-OPh. Bax translocation into mitochondria, efflux of cytochrome c into the cytoplasm, and activation of caspases 9 and 3 between approximately 8 and 12 h p.i. (all hallmarks of the intrinsic apoptotic pathway) were transiently inhibited by expression of Bcl-2, which is not expressed in M1-D cells. Thus, BeAn virus infection in M1-D macrophages, which restricts virus replication, provides a potential mechanism for modulating TMEV neurovirulence during persistence in the mouse central nervous system.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.