Vascular Programs in Emerging and Re-Emerging RNA Virus Infections: Comparative Lessons from SARS-CoV-2, Flaviviruses, and Hantaviruses.

Authors

Silvia Beltrami, Giovanni Strazzabosco, Giovanna Schiuma, Sabrina Rizzo, Marcello Baroni, Daria Bortolotti

Published in

Viruses. Volume 18. Issue 10. Oct 19, 2026. Epub Oct 19, 2026.

Abstract

Emerging and re-emerging RNA viruses frequently present with clinical phenotypes that extend beyond classical organ tropism and include vascular leakage, platelet dysregulation, coagulation imbalance, microvascular injury, and thromboinflammation. SARS-CoV-2, flaviviruses, and hantaviruses provide three complementary models of virus-induced vascular disease. This narrative review compares these viruses through a shared endothelial-coagulative framework and proposes four partially overlapping vascular programs: endothelial activation, endothelial barrier failure, coagulation activation, and platelet quantitative or qualitative dysfunction. These programs are intended as a conceptual synthesis of convergent clinical, pathological, and experimental evidence rather than as a quantitative classification system. The framework is used not only to organize known mechanisms, but also to generate testable predictions for cross-virus biomarker panels, organ-specific endothelial models, and phenotype-guided clinical studies. Severe COVID-19 illustrates inflammation-driven endothelial activation, platelet-leukocyte interactions, complement amplification, NETosis, and immunothrombosis. Within the flavivirus group, DENV is used as the principal model for systemic vascular leakage, thrombocytopenia, and hemorrhagic risk; selected non-dengue flaviviruses illustrate how shared endothelial, platelet, and coagulation modules are redirected toward placental dysfunction (ZIKV), neuroinvasion (WNV and JEV), or hepatic failure and coagulopathy (YFV). Hantavirus infections provide a distinctive model of capillary leak syndrome in which non-lytic endothelial infection, immune-mediated injury, and permeability signaling converge on renal and pulmonary microvascular beds. A comparative view suggests that thrombotic, hemorrhagic, and leaky phenotypes are not mutually exclusive categories, but different outcomes of overlapping vascular programs shaped by viral tropism, vascular-bed specialization, immune activation, and host susceptibility.

PMID:
42944079
Bibliographic data and abstract were imported from PubMed on 27 Oct 2026.

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