The circulatory and immune systems function in close coordination to maintain homeostasis and act as a frontline defense against infections. However, under certain conditions, this interaction becomes dysregulated, leading to thromboinflammation, a pathological process marked by the concurrent and excessive activation of coagulation, inflammation, and endothelial dysfunction. During viral infections, this phenomenon can markedly worsen clinical outcomes. Evidence indicates that viruses such as dengue, chikungunya, influenza, and SARS-CoV can trigger thromboinflammatory responses involving platelet activation, the release of procoagulant and pro-inflammatory mediators, and the formation of thrombi within blood vessels. While this response may initially help contain viral dissemination, in cases of high viremia it can progress to disseminated intravascular coagulation (DIC), hemorrhage, and multiple organ failure. This review compiles current evidence on thromboinflammatory mechanisms induced by arboviral and respiratory viruses and examines how these processes contribute to diseases’ pathogenesis and clinical severity.
Batista et al. (Wed,) studied this question.