"Snakebite envenoming is a neglected tropical disease that disproportionately affects populations in rural tropical regions, with sub-Saharan Africa bearing a substantial burden. It is estimated that more than 300,000 snakebites occur annually in this region, leading to over 7,000 deaths and 10,000 amputations, although the actual incidence and mortality may be up to 5 times higher1,4 (Fig. 1a). Currently, the only specific treatment for snakebite envenoming is antivenoms derived from the plasma of hyperimmunized large animals, such as horses."
"Although they are life-saving, these antivenoms suffer from batch-to-batch variation, high production costs, sometimes restricted efficacy across species (that is, limited polyvalency), and the risk of causing immunological adverse reactions. In addition, existing antivenoms may contain as little as 10% active ingredient-that is, antibodies specifically neutralizing venom toxins7. Consequently, large doses need to be administered, increasing treatment costs. Furthermore, current antivenoms are often ineffective at mitigating local tissue damage caused by envenoming, such as dermonecrosis,"
Sub-Saharan Africa experiences a high burden of snakebite envenoming, with >300,000 bites annually, thousands of deaths, and many amputations, and true numbers may be up to five times higher. Traditional antivenoms are produced from hyperimmunized large-animal plasma and are life-saving but show batch variation, high production costs, limited cross-species efficacy, low proportions of toxin-neutralizing antibodies, and risk of immunological adverse reactions. An experimental recombinant antivenom pipeline used an alpaca and a llama immunized with venoms from 18 elapid snakes to generate VHH-displaying phage libraries. Broadly cross-reactive, high-affinity VHHs were identified, characterized in vitro and in vivo, and eight VHHs were combined into an experimental recombinant antivenom.
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