Abstract

Background: Micronutrient selenium (Se) is an antioxidant. Previous research determined that Se-deficient hosts (<1·2 µMol Se, assayed in blood) infected with benign forms of some RNA viruses (coxsackievirus B3, influenza A virus H2N2) became immunocompromised and that those RNA viruses mutated rapidly, often to virulence. Adequate Se-supplementation to the was found to improve immunocompetence and curtail rapid virus mutation. Initial mapping correlated geographic origins of five RNA viruses and emergence of associated viral infectious diseases (VIDs) with global regions low in Se available to subsistence crops and diet. Method: Information and data, from PubMed, were synthesized to understand geochemical, ecological, and biomolecular causative mechanisms underlying correlations between Se-deficient status, RNA virus activity, and emergence of associated VIDs. Findings: Infecting viruses induce oxidative stress in Se-deficient hosts, e.g., protein cysteine (Cys-S-) residues over-oxidize (e.g., Cys-S- + 3O- → Cys-SO3-), causing antiviral proteins to malfunction. Virulent virus mutations further hijack the host's immune system. Ecological and etiological pathways of virulence for 11 contemporary viruses were tracked. Some virulence mechanisms for several viruses (e.g., HIV/AIDS, Ebola, chikungunya, Zika microcephaly, various influenzas) were identified. Interpretation: The RNA viruses cited demonstrate previously identified fundamental of infectious diseases, including host to infection and microbial/viral change and adaptation. Confounding determinants of commerce and conflict add to virus distribution and to susceptibility to infection. In part, global to RNA virus expression can be monitored by blood-Se assay. Remediation against emergence of RNA VIDs has been demonstrated with access to adequate nutritional Se. Funding Statement: The authors declare N/A (None). Declaration of Interests: The authors state: No conflict of interest.

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