Envenoming by snake bite is recorded unsystematically. The World Health Organization reports that more than 5 million people are bitten by snakes annually. They estimate that up to 138,000 die of complications, and many victims are left disabled. Stazi et al. developed a mouse model of envenoming by the Papuan taipan (Oxyuranus scutellatus). This snake’s poison, taipoxin, is a phospholipase A2 neurotoxin akin to tetanus and botulinum toxins. Taipoxin causes the degeneration of motor axon synaptic transport but does not kill the neurons, and a slow recovery occurs if the victim is given respiratory support. Signaling by the G protein–coupled receptor CXCR4 is implicated in this synaptic pathophysiology. The authors studied the effects of a previously identified agonist of CXCR4, NUCC-390, a nontoxic compound in mice that accelerates regeneration of their synapses, and found that it significantly accelerated recovery from paralysis. NUCC-390 thus has the potential to enhance the recovery of patients hospitalized with neuroparalytic snake envenomation.
PLOS Negl. Trop. Dis. 14, e0008547 (2020).