ReviewVirulence2026
Hijacking and subversion of macrophage antiviral functions by viruses.
Review in Virulence, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
No grant is acknowledged in the PubMed record.
Abstract
Macrophages are frontline effectors of innate immunity, acting as essential elements for clearing pathogens. However, viruses have continuously evolved sophisticated mechanisms to subvert these critical defenses. This review comprehensively decodes how viral pathogens systematically dismantle macrophage microbicidal capacities. It delineates the evasion of pattern recognition receptor surveillance, the hijacking of endocytic trafficking, and the active arrest of phagolysosomal maturation to secure intracellular replication niches. Furthermore, the review explores the paradoxical viral manipulation of the host oxidative burst, where pathogens weaponize reactive oxygen species or exploit antioxidant machineries, driving severe redox dysregulation. Profound metabolic reprogramming, including shifts toward aerobic glycolysis and the skewing of inflammatory polarization alongside cell death pathways, is also examined. Ultimately, these evasion strategies inflict functional paralysis on macrophages, heavily predisposing hosts to severe secondary bacterial coinfections. Mapping this virus-host crosstalk highlights critical vulnerabilities, providing a foundation for novel host-directed antiviral immunotherapies.
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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 Socratic graph.