Daboia russelii siamensis phospholipase A2 toxins (Ds-PLA2)

Daboia russelii siamensis phospholipase A2 (PLA2) toxins are a diverse family of proteins that constitute a major portion of the venom of the Eastern Russell's Viper (Daboia siamensis) [1, 2]. These toxins, which include both enzymatically active and inactive isoforms such as Daboiatoxin and RvPLA2, are primarily responsible for the severe systemic effects observed during envenomation [3, 4]. They function by catalyzing the hydrolysis of the sn-2 ester bond in phospholipids, leading to membrane disruption and the release of bioactive lipids that trigger inflammatory cascades [2, 5]. Clinically, these toxins induce pre-synaptic neurotoxicity, systemic myotoxicity, and are a leading cause of acute kidney injury (AKI) in snakebite victims across Southeast Asia [2, 6]. Because of their central role in venom toxicity, they are primary targets for therapeutic intervention [1, 7]. Current treatments include the administration of specific antivenoms and the investigation of small-molecule inhibitors like Varespladib, which aim to neutralize the enzymatic activity and prevent the progression of tissue damage and paralysis [7, 8].

Other names

Daboia siamensis phospholipase A2DaboiatoxinRvPLA2Drs-PLA2Eastern Russell's viper PLA2Snake venom phospholipase A2svPLA2U1-viperitoxin-Dr1aU1-viperitoxin-Dr1b

Inhibition of the enzymatic activity of secretory phospholipase A2 (sPLA2) to prevent the hydrolysis of cell membrane phospholipids and the subsequent release of inflammatory and toxic mediators.