ArticlePLoS neglected tropical diseases2025
Unveiling the cardiovascular impact of Zika Virus: Myocardial injury, prothrombotic state, and oxidative stress in immunocompetent mice.
Article in PLoS neglected tropical diseases, 2025. 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
11 authors.
Funding
Abstract
The Zika virus (ZIKV) has been associated with neurological and cardiovascular complications, including myocarditis, arrhythmias and thrombotic events. This study evaluated the thrombotic and oxidative responses induced by ZIKV in cardiac cells and immunocompetent mice. Cardiac (H9c2) and vascular smooth muscle (A7r5) cell lines were infected with ZIKV and analyzed for viral replication, cytopathic effects and oxidative stress. In vivo, female FVB/N mice were inoculated with ZIKV and cardiac tissue was analyzed for markers of myocardial damage, prothrombotic enzymes and oxidative stress. H9c2 cells demonstrated higher viral replication and cytopathic effects than A7r5 cells. ZIKV-infected cells exhibited increased lactate dehydrogenase release and oxidative stress markers, including elevated protein carbonylation and reactive oxygen species. In vivo, infected mice displayed significant increases in cardiac troponin T levels, indicative of myocardial injury. Analysis of cardiac tissue revealed elevated thrombin and Factor Xa activities and reduced plasmin, indicating a prothrombotic state. Oxidative stress was marked by increased activities of antioxidant enzymes (GPx, SOD) and reduced glutathione levels, alongside heightened protein oxidation. This study demonstrates that ZIKV infection disrupts cardiovascular homeostasis by inducing myocardial injury, prothrombotic state and oxidative stress. These findings underscore the potential of ZIKV to affect the cardiovascular system beyond its established neurotropism, highlighting the need for further investigation into its systemic impacts.
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.