A Biophysical Approach to SARS-CoV-2 Pathogenicity

In order to infect the target host cell, a virus like severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), whose lytic/virulent lifestyle involves the infection, replication and lysis of the host cell, must be able to penetrate its membrane for the release of viral progeny. For this purpose, its action takes place both on a biophysical and biochemical level. Viral action begins with the alteration of physiological interactions held by the target cell with extracellular aqueous electrolytic solutions (membrane-ions interactions), followed by the disruption of the membrane structural properties. In the present paper the earliest virus-host biophysical events are addressed, in particular the electrostatic (short-range) and electrodynamic (long-range) interactions. In section one a biophysical profile of SARS-CoV-2 pathogenicity is outlined. The prominent electrostatic events that characterize the earliest stages of virus-host interactions are taken into account. The host cell oxidative stress reaction is discussed. In section two, biological water as biphasic liquid and structured interfacial water’s fourth phase are introduced by resorting to Quantum Field Theory (QFT) and Quantum Electrodynamic (QED). Structured interfacial water as a semiconductor and the proton-based self-driven liquid-flow system are also discussed. In section three it is assumed that in its approach to the target host cell SARS-CoV-2 triggers the cellular phase-matching feature (which operates as a very selective filter discriminating among perturbations and stimuli that are out of phase with the oscillatory motions allowed by the cell’s inner dynamics) by emitting a stressful ultra low frequency-electromagnetic field (ULF-EMF), which generates an alert response within the cell by influencing ionic fluxes throughout cellular membrane. Therefore, it is suggested that the earliest virus-host interaction would rest on electromagnetic long-range events, before electrostatic and chemical interactions occur, which are influencing the redox potential of the target host-cell’s membrane chemical species, affecting its acid-base equilibria, therefore inducing a cellular stress response (e.g. via plasma-membrane-localized redox signalling) with reactive oxygen species (ROS) and reactive nitrogen species (RNS) production. Accordingly, redox-responsive intracellular signaling and anti-inflammatory scavenging systems would be remotely (pre) activated by non-ionizing interference phenomena, before virus-cell come together, followed by electrostatic and chemical events that provoke a branching, cascade-like, chain of reactions. A better understanding of the earliest of biophysical events will enable a more rational approach to dealing with both the binding of the SARS-CoV-2 highly glycosylated Spike’s S1 subunit receptor binding domain (RBD) to the host cell’s angiotensin-converting enzyme 2 (ACE2) and the direct interaction with the lipid bilayer on the cell surface.