SARS-CoV-2 is a newly identified coronavirus that causes the respiratory disease called coronavirus disease 2019 (COVID-19). With an urgent need for therapeutics, we lack a full understanding of the molecular basis of SARS-CoV-2-induced cellular damage and disease progression. Here, we conducted transcriptomic analysis of human PBMCs, identified significant changes in mitochondrial, ion channel, and protein quality-control gene products. SARS-CoV-2 proteins selectively target cellular organelle compartments, including the endoplasmic reticulum and mitochondria. M-protein, NSP6, ORF3A, ORF9C, and ORF10 bind to mitochondrial PTP complex components cyclophilin D, SPG-7, ANT, ATP synthase and a previously undescribed CCDC58 (Coiled-coil domain containing protein 58). Knockdown of CCDC58 or mPTP blocker cyclosporin A pretreatment enhances mitochondrial Ca 2+ retention capacity and bioenergetics. SARS-CoV-2 infection exacerbates cardiomyocyte autophagy and promotes cell death that was suppressed by cyclosporin A treatment. Our findings reveal that SARS-CoV-2 viral proteins suppress cardiomyocyte mitochondrial function that disrupts cardiomyocyte Ca 2+ cycling and cell viability.

An elementary model consisting of one charged particle in a viscous medium exposed to weak ac-dc low-frequency magnetic fields is analyzed to identify and explain the fundamental characteristics of the physical mechanisms that result in a resonance response, which is similar to the familiar cyclotron resonance. The model predicts both frequency and amplitude windows, which are explained in terms of synchronization of the particle with electric fields. Although extrapolation of model results to biological systems is limited by the elementary nature of the model, the model results indicate that observed resonant responses by others of biological systems to ac-dc magnetic fields are probably not due to resonant response of ions in solution, since the model predicts that no resonant response is possible unless the viscous damping is very low, many orders of magnitude lower than the viscous damping of ions in solution.

Observations recently reported by others indicate that a combination of a weak dc magnetic field and extremely-low-frequency ac magnetic field can produce resonant effects in biological systems. We report measurements of the effects of combined dc and ac magnetic fields on the dc current through channel-free planar phospholipid membranes. The combined dc-ac magnetic fields did affect the dc current through planar phospholipid membranes, but not in every membrane, and not consistently at the same values of magnetic flux density and frequency. None of our measurements showed resonant response akin to the cyclotron-like resonance reported in diatoms [Smith et al., 1987] and lymphocytes [Liboff et al., 1987].