ABSTRACT
The SARS-CoV-2 virus is primarily transmitted through direct or indirect contact with the mucous membranes of the mouth and nostrils. The presence of SARS-CoV-2 in sputum with a high viral load suggested that maintaining good oral hygiene could be critical in limiting COVID-19 disease. Brushing the teeth frequently and regularly with widely available amphiphilic detergent, sodium lauryl sulfate (SLS)-based toothpastes could help in preventing the spread of SARS-CoV-2. We proposed a community survey-based methodology followed by an in vitro biochemical strategy to test the virucidal potentiality of SLS, an amphiphilic detergent found in these toothpastes. Through biomolecular structure and docking analysis using models of spike protein and SLS, we showed a possible molecular mechanism of action for SLS-enabled viral particle inactivation.
ABSTRACT
The novel SARS-CoV-2virus that caused the disease COVID-19 is currently a pandemic worldwide. The virus requires an alveolar type-2 pneumocyte in the host to initiate its life cycle. The viral S1 spike protein helps in the attachment of the virus on toACE-2 receptors present on type-2 pneumocytes, and the S2 spike protein helps in the fusion of the viral membrane with the host membrane. Fusion of the SARS-CoV-2virus and host membrane is followed by entry of viral RNA into the host cells which is directly translated into the replicase-transcriptase complex (RTC) following viral RNA and structural protein syntheses. As the virus replicates within type-2 pneumocytes, the host immune system is activated and alveolar macrophages start secreting cytokines and chemokines, acting as an inflammatory mediator, and chemotactic neutrophils, monocytes, natural NK cells, and CD8+ T cells initiate the local phagocytosis of infected cells. It is not the virus that kills COVID-19 patients; instead, the aberrant host immune response kills them. Modifying the response from the host immune system could reduce the high mortality due to SARS-CoV-2 infection. The present study examines the viral life cycle intype-2 pneumocytes and resultant host immune response along with possible therapeutic targets.