# Unveiling the cardiovascular impact of Zika Virus: Myocardial injury, prothrombotic state, and oxidative stress in immunocompetent mice

## TL;DR

This study shows that the Zika virus can damage the heart, increase blood clotting risk, and cause chemical stress in mice, beyond its known effects on the nervous system.

## Contribution

The study reveals new cardiovascular effects of ZIKV in immunocompetent mice, including myocardial injury, prothrombotic state, and oxidative stress.

## Key findings

- ZIKV replicates in cardiac cells, causing damage and oxidative stress.
- Infected mice showed elevated cardiac troponin T, indicating heart muscle injury.
- ZIKV induced a prothrombotic state with increased thrombin and Factor Xa activities.

## 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.

Zika virus (ZIKV) is widely known for its neurological complications, especially in newborns. However, this study reveals that ZIKV can also cause significant effects on the heart. Researchers investigated the impact of ZIKV infection on cardiac cells and healthy immunocompetent mice. They found that the virus is able to replicate in heart cells, leading to cellular damage and oxidative stress, a harmful chemical imbalance in the body. In infected mice, clear signs of heart muscle injury were observed, along with increased levels of clotting-related enzymes, suggesting a higher risk of thrombotic events such as heart attacks or strokes. The study also detected elevated antioxidant responses, indicating the body’s attempt to counteract virus induced stress. These findings demonstrate that ZIKV infection can disrupt cardiovascular function, causing myocardical injury, a prothrombotic state, and oxidative stress. This work expands our understanding of ZIKV’s effects beyond the nervous system and highlights the need for further research into the virus’s systemic impact on human health.