ArticleVirology2013
Multiplicity-dependent activation of a serine protease-dependent cytomegalovirus-associated programmed cell death pathway.
Article in Virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Review
- A Cysteine Residue of Human Cytomegalovirus vMIA Protein Plays a Crucial Role in Viperin Trafficking to Control Viral Infectivity.Journal of virology · 2023Article
- Programmed Necrosis in Host Defense.Current topics in microbiology and immunology · 2023Article
- Article
- THY-1 Cell Surface Antigen (CD90) Has an Important Role in the Initial Stage of Human Cytomegalovirus Infection.PLoS pathogens · 2015Article
- Suppression of RIP3-dependent necroptosis by human cytomegalovirus.The Journal of biological chemistry · 2015Article
- Interplay of autophagy and apoptosis during murine cytomegalovirus infection of RPE cells.Molecular vision · 2014Article
- Transcription of true late (γ2) cytomegalovirus genes requires UL92 function that is conserved among beta- and gammaherpesviruses.Journal of virology · 2014Article
- Cytomegalovirus UL91 is essential for transcription of viral true late (γ2) genes.Journal of virology · 2013Article
- Viral modulation of programmed necrosis.Current opinion in virology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
At a low MOI (≤0.01), cytomegalovirus-associated programmed cell death terminates productive infection via a pathway triggered by the mitochondrial serine protease HtrA2/Omi. This infected cell death is associated with late phase replication events naturally suppressed by the viral mitochondrial inhibitor of apoptosis (vMIA). Here, higher MOI (ranging from 0.1-3.0) triggers cell death earlier during infection independent of viral DNA synthesis. Thus, MOI-dependent activating signals early, at high MOI, or late, at low MOI, during replication promote serine protease-dependent death that is suppressed by vMIA. Treatment with an antioxidant targeting reactive oxygen species (ROS) or the serine protease inhibitor N-alpha-p-tosyl-L-lysine chloromethyl ketone (TLCK) delays cell death, and the combination has an additive impact. These studies identify serine proteases and ROS as important factors triggering programmed cell death induced by vMIA-deficient virus, and show that this death pathway occurs earlier and reduces viral yields as the MOI is increased.
Indexed as
Identifiers
What OpenQuestion holds
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.