ArticleJournal of virology2010
Viral cell death inhibitor MC159 enhances innate immunity against vaccinia virus infection.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Molluscum Contagiosum Virus: Biology and Immune Response.Advances in experimental medicine and biology · 2024Review
- Poxviruses and the immune system: Implications for monkeypox virus.International immunopharmacology · 2022Review
- Interaction between the Hepatitis B Virus and Cellular FLIP Variants in Viral Replication and the Innate Immune System.Viruses · 2022Review
- Molluscum Contagiosum Virus MC159 Abrogates cIAP1-NEMO Interactions and Inhibits NEMO Polyubiquitination.Journal of virology · 2017Article
- RIPK1 and PGAM5 Control Leishmania Replication through Distinct Mechanisms.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Necroptosis-independent signaling by the RIP kinases in inflammation.Cellular and molecular life sciences : CMLS · 2016Review
- Functional Comparison of Molluscum Contagiosum Virus vFLIP MC159 with Murine Cytomegalovirus M36/vICA and M45/vIRA Proteins.Journal of virology · 2015Article
- Murine cytomegalovirus virion-associated protein M45 mediates rapid NF-κB activation after infection.Journal of virology · 2014Article
- Staying alive: cell death in antiviral immunity.Molecular cell · 2014Review
- Inhibition of interferon gene activation by death-effector domain-containing proteins from the molluscum contagiosum virus.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Vaccinia virus induces programmed necrosis in ovarian cancer cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2013Article
- CYLD deubiquitinates RIP1 in the TNFα-induced necrosome to facilitate kinase activation and programmed necrosis.PloS one · 2013Article
- Caspase-8 and FLIP regulate RIG-I/MDA5-induced innate immune host responses to picornaviruses.Future virology · 2012Article
- High-dimensional gene expression profiling studies in high and low responders to primary smallpox vaccination.The Journal of infectious diseases · 2012Article
- Article
- The MC159 protein from the molluscum contagiosum poxvirus inhibits NF-κB activation by interacting with the IκB kinase complex.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- cIAPs block Ripoptosome formation, a RIP1/caspase-8 containing intracellular cell death complex differentially regulated by cFLIP isoforms.Molecular cell · 2011Article
- Modulation of NF-κB signalling by microbial pathogens.Nature reviews. Microbiology · 2011Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
Viral inhibitors of host programmed cell death (PCD) are widely believed to promote viral replication by preventing or delaying host cell death. Viral FLIPs (Fas-linked ICE-like protease [FLICE; caspase-8]-like inhibitor proteins) are potent inhibitors of death receptor-induced apoptosis and programmed necrosis. Surprisingly, transgenic expression of the viral FLIP MC159 from molluscum contagiosum virus (MCV) in mice enhanced rather than inhibited the innate immune control of vaccinia virus (VV) replication. This effect of MC159 was specifically manifested in peripheral tissues such as the visceral fat pad, but not in the spleen. VV-infected MC159 transgenic mice mounted an enhanced innate inflammatory reaction characterized by increased expression of the chemokine CCL-2/MCP-1 and infiltration of γδ T cells into peripheral tissues. Radiation chimeras revealed that MC159 expression in the parenchyma, but not in the hematopoietic compartment, is responsible for the enhanced innate inflammatory responses. The increased inflammation in peripheral tissues was not due to resistance of lymphocytes to cell death. Rather, we found that MC159 facilitated Toll-like receptor 4 (TLR4)- and tumor necrosis factor (TNF)-induced NF-κB activation. The increased NF-κB responses were mediated in part through increased binding of RIP1 to TNFRSF1A-associated via death domain (TRADD), two crucial signal adaptors for NF-κB activation. These results show that MC159 is a dual-function immune modulator that regulates host cell death as well as NF-κB responses by innate immune signaling receptors.
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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.