Micronutrient Status and Host Defense Against Infectious Diseases: Mechanisms, Clinical Evidence, and...

Micronutrients support epithelial barrier integrity, innate immune activity, adaptive immune responses, and redox regulation. However, micronutrient deficiency and supplementation do not have uniform relationships with infectious-disease risk or clinical outcomes.

This review examines the mechanisms linking micronutrient status with host defence and evaluates clinical evidence for micronutrient interventions across gastrointestinal, respiratory, systemic viral, bacterial, and parasitic infections.

Vitamins A, C, D, and E, together with zinc, selenium, and iron, influence epithelial barriers, phagocyte activity, lymphocyte function, cytokine regulation, oxidative stress, and pathogen-host nutrient competition. Clinical evidence is context-dependent. In randomised trials in children in low- and middle-income settings, therapeutic zinc was associated with shorter diarrhoeal duration, whereas findings for respiratory infections vary according to population, baseline status, intervention, and outcome. Vitamin D supplementation was associated with a modest reduction in acute respiratory infection risk in some randomised trials, but effects are not uniform across settings, and later aggregate-data meta-analyses did not confirm the earlier subgroup findings. Iron needs particular caution because deficiency can impair host defence, whereas excess available iron was associated with increased infection risk in some settings.

Evaluate micronutrient interventions by baseline nutritional status, infection type, dose, timing, concurrent treatment, outcome definition, and safety. Future studies should prioritise stratified trials, standardised outcomes, transparent reporting, and targeted supplementation over universal high-dose approaches.