ArticlePLoS pathogens2008
HtrA2/Omi terminates cytomegalovirus infection and is controlled by the viral mitochondrial inhibitor of apoptosis (vMIA).
Article in PLoS pathogens, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 51 citations in OpenAlex.
- Host proteases: key regulators in viral infection and therapeutic targeting.Frontiers in immunology · 2025Review
- Review
- No Time to Die: How Cytomegaloviruses Suppress Apoptosis, Necroptosis, and Pyroptosis.Viruses · 2024Review
- Protease-independent control of parthanatos by HtrA2/Omi.Cellular and molecular life sciences : CMLS · 2023Article
- Programmed Necrosis in Host Defense.Current topics in microbiology and immunology · 2023Article
- Article
- TNF Signaling Dictates Myeloid and Non-Myeloid Cell Crosstalk to Execute MCMV-Induced Extrinsic Apoptosis.Viruses · 2020Article
- Human Cytomegalovirus pUL37x1 Is Important for Remodeling of Host Lipid Metabolism.Journal of virology · 2019Article
- Review
- Real-Time Visualization and Quantification of Human Cytomegalovirus Replication in Living Cells Using the ANCHOR DNA Labeling Technology.Journal of virology · 2018Article
- The mitochondrial protease HtrA2 restricts the NLRP3 and AIM2 inflammasomes.Scientific reports · 2018Article
- Cytomegalovirus-Infected Cells Resist T Cell Mediated Killing in an HLA-Recognition Independent Manner.Frontiers in microbiology · 2016Article
- Superresolution imaging of human cytomegalovirus vMIA localization in sub-mitochondrial compartments.Viruses · 2014Article
- The proteases HtrA2/Omi and UCH-L1 regulate TNF-induced necroptosis.Cell communication and signaling : CCS · 2013Article
- Viral modulation of programmed necrosis.Current opinion in virology · 2013Review
- Gene products of the embedded m41/m41.1 locus of murine cytomegalovirus differentially influence replication and pathogenesis.Virology · 2013Article
- Multiplicity-dependent activation of a serine protease-dependent cytomegalovirus-associated programmed cell death pathway.Virology · 2013Article
- Viral mitochondria-localized inhibitor of apoptosis (UL37 exon 1 protein) does not protect human neural precursor cells from human cytomegalovirus-induced cell death.The Journal of general virology · 2012Article
- Prevention of cellular suicide by cytomegaloviruses.Viruses · 2012Review
- Inhibition of human cytomegalovirus immediate-early gene expression by cyclin A2-dependent kinase activity.Journal of virology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Viruses encode suppressors of cell death to block intrinsic and extrinsic host-initiated death pathways that reduce viral yield as well as control the termination of infection. Cytomegalovirus (CMV) infection terminates by a caspase-independent cell fragmentation process after an extended period of continuous virus production. The viral mitochondria-localized inhibitor of apoptosis (vMIA; a product of the UL37x1 gene) controls this fragmentation process. UL37x1 mutant virus-infected cells fragment three to four days earlier than cells infected with wt virus. Here, we demonstrate that infected cell death is dependent on serine proteases. We identify mitochondrial serine protease HtrA2/Omi as the initiator of this caspase-independent death pathway. Infected fibroblasts develop susceptibility to death as levels of mitochondria-resident HtrA2/Omi protease increase. Cell death is suppressed by the serine protease inhibitor TLCK as well as by the HtrA2-specific inhibitor UCF-101. Experimental overexpression of HtrA2/Omi, but not a catalytic site mutant of the enzyme, sensitizes infected cells to death that can be blocked by vMIA or protease inhibitors. Uninfected cells are completely resistant to HtrA2/Omi induced death. Thus, in addition to suppression of apoptosis and autophagy, vMIA naturally controls a novel serine protease-dependent CMV-infected cell-specific programmed cell death (cmvPCD) pathway that terminates the CMV replication cycle.
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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.