2026-07-11 | Coagulopathy in viral haemorrhagic fevers and beyond: molecular mechanisms and targeted interventions.

Coagulopathy refers to any medical condition which affects the ability of the blood to clot. It can be caused due to genetic conditions like haemophilia, von Willebrand disease, or it can be caused through liver disease or deficiency of Vitamin K. It also involves a broad range of diseases affecting hemostasis as an unbalanced and even bidirectional relationship between thrombosis and bleeding. Coagulopathy can also be caused by thromboinflammation, as seen in VHFs like Ebola, Dengue, Marburg, Crimean-Congo Hemorrhagic Fever, Yellow Fever, and Hantavirus infection. The immune response and coagulation system are intricately linked in such cases. Infections from VHFs cause endothelial cell dysfunction through the immune response, monocytes/macrophages activation, and increased expression of tissue factor (TF), which in turn causes excessive thrombin production and fibrin formation. These conditions result in microvascular thrombosis, organ dysfunction, consumption of platelets and coagulation factors, causing a balanced but fragile state of hemostasis that could tip over towards either thrombosis or bleeding. New therapies have been developed that interfere with these processes, such as interference with the TF pathway (for instance, rNAPc2) and regulation of fibrinolysis (tranexamic acid). The recognition of the double-edged sword of coagulopathy is critical for the development of treatment strategies targeting coagulation disorders. This literature review discusses the molecular basis of immunothrombosis and endothelial dysfunction in VHFs.

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2026-06-30 | Ebola Virus Disease: What We Know, How Deadly It is, and How It Spreads Compared to COVID-19?

Prevention (CDC) noting that, without treatment, up to 90% of cases can be fatal. 10Across outbreaks, the WHO summarizes an average CFR of around 50% and emphasizes wide variability (25-90%) in past outbreaks. 4 Syntheses of multiple outbreaks also find high overall lethality.A meta-analysis covering 42 outbreaks (1976-2022) reported a pooled CFR of 60.6% (95% CI 51.6-69.4) and estimated that the CFR declined over time but stabilized at around 61.0% (95% CI 52.0-69.0) between 2014 and 2022. 13Another meta-analysis reported an overall CFR estimate of 65.4% (95% CI 54.6-75.5),with substantial variation among outbreaks. 14The European Centre for Disease Prevention and Control (ECDC) similarly cites a weighted CFR of 65.0% (95% CI 54.0-76.0)and highlights higher fatality for Zaire ebolavirus (75%) than for Sudan ebolavirus (53%). 2 Lethality differs by virus species.In the 1976-2022 metaanalysis, Zaire virus had the highest CFR estimate (66.6%), followed by Sudan virus (48.5%),Bundibugyo virus (32.8%), and Taï Forest virus (0%). 13linical features associated with mortality (useful for triage and clinical monitoring) have been summarized in pooled analyses; fatal cases more often had bleeding events, vomiting, diarrhea, and abdominal pain than survivors in one meta-analysis of clinical findings. 15 How deadly I S It?Severity is driven by both the clinical syndrome and the historically high fatality rate, with the Centers for Disease Control and

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2026-06-28 | A New Proposal for Host-Directed Therapy in Ebola Virus Disease: Ozone Autohemotherapy as an Adjunctive Approach Within a Systems Biology Framework

Ebola Virus Disease (EVD) remains one of the most lethal viral hemorrhagic fevers, with mortality driven not only by viral replication but also by a dysregulated host response characterized by hyperinflammation, endothelial dysfunction, coagulopathy, metabolic derangement and multi-organ failure. Although monoclonal antibodies and vaccination have substantially improved outcomes, currently available interventions primarily target the virus and do not directly address the complex host-response networks that contribute to advanced disease and mortality. Here, we propose a systems biology framework for evaluating Ozone Autohemotherapy (O₃-AHT), specifically Major Autohemotherapy (MAH), as a host-directed adjunctive strategy in EVD. The framework is based on the capacity of O₃-AHT to generate controlled redox signals through Reactive Oxygen Species (ROS) and Lipid Ozonation Products (LOPs), which activate adaptive stress-response pathways including the Nrf2/Keap1/Antioxidant Response Element (ARE) system, the AMP-Activated Protein Kinase (AMPK)-Forkhead Box O (FOXO)-mechanistic Target of Rapamycin (mTOR)-sirtuin 1 (Sirt1) axis and Nrf2-mediated modulation of Nuclear Factor Kappa B (NF-κB) signaling. These interconnected pathways regulate antioxidant defenses, mitochondrial adaptation, autophagy, inflammatory responses, endothelial homeostasis and immune regulation-biological processes that intersect with major pathogenic mechanisms of EVD. Particular attention is given to Heme Oxygenase-1 (HO-1), a downstream effector of Nrf2 activation for which experimental evidence demonstrates suppression of Ebola virus replication in-vitro, providing a mechanistic bridge between host-directed redox modulation and antiviral activity. By integrating current knowledge from virology, immunology, redox biology and systems medicine, this framework identifies multiple points of convergence between ozone-induced adaptive signaling and Ebola pathophysiology. This work does not establish clinical efficacy but presents a hypothesis-generating model intended to guide future experimental investigation. As a conceptual framework, it proposes O₃-AHT as a candidate host-directed adjunctive approach that warrants systematic evaluation in preclinical models of Ebola virus disease.

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