Abstract
Snake venoms are mixtures of toxins that vary extensively between and within snake species. This variability has serious consequences for the management of the world’s 1.8 million annual snakebite victims. Advances in ‘omic’ technologies have empowered toxinologists to comprehensively characterize snake venom compositions, unravel the molecular mechanisms that underpin venom variation, and elucidate the ensuing functional consequences. In this review, we describe how such mechanistic processes have resulted in suites of toxin isoforms that cause diverse pathologies in human snakebite victims and we detail how variation in venom composition can result in treatment failure. Finally, we outline current therapeutic approaches designed to circumvent venom variation and deliver next-generation treatments for the world’s most lethal neglected tropical disease.
Highlights
The consequences of such human snakebites can be severe
Concluding Remarks Toxin-encoding genes are members of some of the most dynamically evolving gene families found in nature and detailed studies of their molecular evolution can yield knowledge that is broadly applicable to the deepest questions in biology, those concerning the origins of novel functions [2,3,4,5]
Whilst this evolutionary dynamism makes toxins an attractive research subject for molecular biologists, it has led to the creation of a pharmacologically diverse suite of toxic molecules that are the causative agents for the monumental clinical burden of snakebite envenoming observed today [10]
Summary
The consequences of such human snakebites can be severe. Current estimates suggest that venomous snakes cause up to 138 000 deaths worldwide each year and perhaps as many as 500 000 additional cases of venom-induced morbidity [10]. Variation in toxin venom components occurs both inter- and intraspecifically as the result of various processes, including gene duplication and the action of positive selection.
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