Abstract
In this paper we present a new approach to the mechanism of inactivation of enveloped virus aerosols. The analysis is in terms of oxidation of the lipid bilayer of the viral envelope through a free radical chain reaction. The rate kinetics of the process for various enveloped viruses have been compared and the indications are that the inactivations are closely related. Promoting virus inactivation with UV light is briefly reviewed and discussed as an extension of the chain reaction mechanism, which with physicochemical analyses give insights into the process and of reaction complexities. An outline of a practical method of achieving a 3-log10 level of deactivation in 1 min is described with purified air being returned to healthcare environments.
Highlights
We have carried out an analysis of the inactivation of enveloped viruses in general and of SARS-CoV-19 in particular in terms of a suggested decomposition chemistry for the lipid bilayer through a free radical chain reaction
The analysis and the chemical considerations together with the application of the kinetics to other enveloped viruses indicate that the inactivations of such viruses are comparable
Considerations of the chemistry highlight why UV light can be a powerful initiator for virus inactivation, which together with physicochemical analyses give insights into how a 3-log10 level of deactivation in 1 min, or a greater level of inactivation, could be achieved
Summary
Elucidate those roles, studies have been made of the composition of viral envelopes, for example, through the development of lipodomics, a mass spectrometry-based systematic analysis of cellular lipids in general [7]. It is suggested that it is realistic to expect that far-UVC light would show comparable inactivation efficiency against other human coronaviruses, including SARS-CoV-2; that is in accord with our discussion on viral lipid oxidation. Aerosol studies yield higher rate constants than for surface samples and this is because viruses tumbling in the air will receive all round UV exposure while those on surfaces receive exposure in one plane only, and virus samples absorbed into filter papers would be even less accessible to UV light. There is a significant difference for aerosol viral lipid oxidation from that of more usual situations of lipid chain reactions in that, as we have seen and as indicated, virus concentrations are very low. When there is a high dilution of viral lipids and an aqueous aerosol environment, radical recombinations could be expected to be less important There is another way of considering the falloff in inactivation. That will be sufficient to break the bonds we have been discussing Table 1
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