ArticleJournal of virology2025
Human cytomegalovirus-triggered necroptosis is suppressed by sequestration of MLKL in the nucleus of infected monocytes.
Article in Journal of virology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- HIGH DOSE GAMMAHERPESVIRUS INFECTION IN MACROPHAGES RESULTS IN INFLAMMATORY MULTIMODAL CELL DEATH.bioRxiv : the preprint server for biology · 2026Article
- A Potent Inhibitor of Human Cytomegalovirus Infection Works Post-Entry Specifically in Differentiating Myelo-Monocytic Cells.Pathogens (Basel, Switzerland) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
The systemic spread of human cytomegalovirus (HCMV) is associated with severe morbidity and mortality in immunocompromised and immunonaïve patients. Hematogenous dissemination of HCMV to different organ sites is facilitated by peripheral blood monocytes. Circulating monocytes have a short lifespan due, in part, to their intrinsic biological programming to initiate caspase-8-mediated apoptosis upon entry into the circulation from the bone marrow. We previously reported that HCMV extends the lifespan of infected monocytes by blocking procaspase-8 cleavage, yet the precise viral mechanism responsible for suppressing caspase-8 activity remains unknown. Here, we demonstrate that HCMV entry into monocytes rapidly increases the abundance of the anti-apoptotic cellular FLICE-like inhibitory protein long (cFLIP
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Registered trials
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