SARS-CoV-2's close relative came from a copper mine. On the genetics of the following case, GATA genes are implicated in congenital heart disease (USMB search 'gata'):
Claire Bridges, 20, had both her legs amputated after suffering complications from COVID-19 and followers have been floored by her resilience.
nypost.com
Keeping in mind Zelenko's protocol for zinc (previous posts), there is,
'Recent findings with the cardiac transcription factor NKX2.5, TBX5, and GATA4 exemplify the synergy between human genetics and studies of model organisms for understanding the etiology of human congenital heart disease. Numerous point mutations have been identified in Nkx 2.5 in families with atrial septal defects and progressive cardiac conduction abnormalities.
....
Like the NKX2.5 and TBX5 mutations, mutations in the zinc-finger-containing protein GATA4 cause similar atrial and ventricular septal defects in autosomal dominant nonsyndromic human pedigrees. GATA4 or related proteins are essential for cardiogenesis in flies, fish, and mice. Like NKX2.5, GATA4 and TBX5 also form a complex to regulate downstream genes, such as myosin heavy chain (MHC).
Consistent with an important role for such combinatorial interactions, a familial GATA4 point mutation disrupts GATA4's ability to interact with TBX5. Conversely, several human TBX5 mutations disrupt TBX5 interaction with GATA4 suggesting that the two cooperate in cardiac septation events. Confirming a genetic interraction between the two proteins, mice heterozygous for GATA4 and TBX5 mutations are embryonic lethal from a myocardial defect and severe hypoplasia of the endocardial cushion tissue necessary for valvuloseptal development.
....
Although the compendium of septal genes regulated by these transcription factors is unknown, it is intriguing that mutations in human MHC, a direct target of GATA4, TBX5, and NKX2.5, also cause atrial septal defects. This observation suggests a possible mechanism by which these genes cause septation defects.'
(Epstein, Inborn Errors of Development: The Molecular Basis of Clinical Disorders of Morphogenesis, Ch. 10 Molecular Regulation of Cardiogenesis)