Pathophysiological and therapeutic insights into Viperidae envenomation: Mechanisms, clinical manifestations, and advances in antivenom strategies

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By MathKnight - Own work, based on, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=113490046

Pathophysiological and therapeutic insights into Viperidae envenomation: Mechanisms, clinical manifestations, and advances in antivenom strategies

Summary

Viperidae snakes are among the most medically significant venomous reptiles worldwide, responsible for extensive morbidity and mortality in tropical and subtropical regions. Their venoms are complex mixtures of biologically active proteins and peptides that target key physiological systems, notably hemostasis, inflammation, and tissue integrity. The principal enzymatic constituents include serine and metalloproteinases, phospholipases A2, L-amino acid oxidases, and hyaluronidases, all contributing to local necrosis, hemorrhage, and systemic coagulopathy. Toxins such as disintegrins and C-type lectins further modulate platelet aggregation and immune pathways. Clinically, viper envenomation produces a distinct syndrome marked by severe local inflammation, hemorrhage, edema, and potential multi-organ failure. Recent studies reveal that venom-induced oxidative stress and cytokine cascades amplify tissue damage. Antivenom immunotherapy remains the only specific treatment, yet efficacy varies with venom diversity and regional species distribution. Advances in proteomic and immunological research are paving the way for next-generation antivenoms with improved safety and cross-neutralization profiles. This review synthesizes the biochemical, pathophysiological, and therapeutic dimensions of Viperidae envenomation, emphasizing mechanisms of action and highlighting ongoing efforts toward more effective treatments.
Khelfi, A. (2026). Pathophysiological and therapeutic insights into Viperidae envenomation: Mechanisms, clinical manifestations, and advances in antivenom strategies. Toxicologie Analytique et Clinique. https://doi.org/10.1016/j.toxac.2026.01.002