ReviewViruses2026
The Platelet-Virus Axis in Human Disease.
Review in Viruses, 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
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
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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Platelets have traditionally been viewed as passive cellular elements involved in hemostasis and vascular integrity. However, growing evidence over the last decade has radically changed this paradigm, revealing platelets as dynamic immune and inflammatory effectors that actively participate in host-pathogen interactions. In viral infections, platelets are not merely innocent bystanders but represent key players in a bidirectional and tightly regulated platelet-virus axis that influences viral dissemination, immune activation, endothelial dysfunction, and the development of thrombotic and hemorrhagic complications. Several clinically relevant viruses, including SARS-CoV-2, influenza virus, HIV, dengue virus, and viral hemorrhagic fever-associated pathogens, have been shown to directly or indirectly interact with platelets through surface receptors, immune complexes, and inflammatory mediators, leading to platelet activation, phenotypic reprogramming, and accelerated clearance. These processes contribute to the paradoxical coexistence of thrombocytopenia and hypercoagulability that characterizes many severe viral diseases. Moreover, platelets can act as immune sentinels by sensing viral components, releasing cytokines and chemokines, forming platelet-leukocyte aggregates, and modulating both innate and adaptive immune responses, thereby shaping the clinical course of infection. In this review, we synthesize current evidence on the molecular and cellular mechanisms governing virus-platelet interactions, with particular emphasis on their role in immune-thrombosis, endothelial injury, and organ dysfunction. We further discuss the clinical implications of platelet dysregulation in viral infections, including its potential value as a biomarker of disease severity and as a therapeutic target. Understanding the platelet-virus axis provides a unifying framework to explain the thrombo-inflammatory phenotype of viral diseases and may open new avenues for risk stratification and targeted interventions in affected patients.
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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.