Viral Pathophysiology and Post-harvest Vitamin A Erosion Implications for Pediatric Retinol Status in Biofortified Sweetpotato Systems

Abstract

Background: Orange-fleshed sweetpotato (OFSP) is promoted as a biofortified crop for reducing vitamin A deficiency among children and women in low-resource settings. Its public health value depends on the whole delivery chain, from virus-free planting material and genotype selection to processing, storage, preparation, and consumption. Previous versions of the evidence narrative have sometimes implied that sweetpotato virus disease (SPVD) directly destabilizes carotenoids. The available literature supports a more cautious interpretation: SPVD is a proven agronomic and seed-system threat, while post-harvest handling is the strongest demonstrated driver of carotenoid erosion.
Objective: This critical review evaluates whether, how, and at what point’s viral pathophysiology and post-harvest processes compromise the quantity, retention, bioaccessibility, and pediatric vitamin A value of OFSP systems.
Methods: Evidence was synthesized from selected peer-reviewed articles, thesis evidence, and technical guidance on OFSP efficacy, SPVD, genotype-by-environment performance, carotenoid chemistry, processing retention, storage stability, puree value chains, and scaling. Claims were classified as directly supported, indirectly supported, or unresolved.
Findings: Regular intake of boiled and mashed OFSP can improve vitamin A status in children, and 100-125 g of cooked OFSP can contribute substantially to the daily vitamin A needs of young children under suitable conditions. Carotenoid content varies markedly by genotype, location, flesh color, and environment. Boiling and steaming generally show high carotenoid retention, whereas baking, frying, sun drying, poor flour storage, and prolonged storage at ambient temperature can cause substantial losses. Storage studies consistently identify oxygen exposure, temperature, water activity, packaging, and duration as major determinants of provitamin A loss. SPVD and related viral infections reduce productivity, threaten seed systems, and may indirectly lower vitamin A delivery by reducing the availability and quality of marketable roots; however, direct evidence that SPVD causes carotenoid degradation or impaired bioavailability remains limited.
Conclusion: OFSP remains a credible crop-based strategy for vitamin A deficiency control, but its nutritional effect is not an intrinsic property of orange roots alone. It is the outcome of an integrated food system. The most defensible pathway links clean seed systems, SPVD-resistant and high-beta-carotene genotypes, high-retention processing, oxygen- and light-protective storage, appropriate dietary fat and nutrition education. Future studies should directly compare virus-infected and virus-free OFSP genotypes for carotenoid biosynthesis, retention, bioaccessibility, and child retinol outcomes.