The emergence of SARS-CoV-2 lineages and associated antibody responses among asymptomatic individuals in a large university community (preprint)

SARS-CoV-2 (CoV2) infected, asymptomatic individuals are an important contributor to COVID transmission. CoV2-specific immunoglobulin (Ig), as generated by the immune system following infection or vaccination, has helped limit CoV2 transmission from asymptomatic individuals to susceptible populations (e.g. elderly). Here, we describe the relationships between COVID incidence and CoV2 lineage, viral load, saliva Ig levels (CoV2-specific IgM, IgA and IgG) and inhibitory capacity in asymptomatic individuals between Jan 2021 and May 2022. These data were generated as part of a large university COVID monitoring program and demonstrate that COVID incidence among asymptomatic individuals occurred in waves which mirrored those in surrounding regions, with saliva CoV2 viral loads becoming progressively higher in our community until vaccine mandates were established. Among the unvaccinated, infection with each CoV2 lineage (pre-Omicron) resulted in saliva Spike-specific IgM, IgA and IgG responses, the latter increasing significantly post-infection and being more pronounced than N-specific IgG responses. Vaccination resulted in significantly higher Spike-specific IgG levels compared to unvaccinated infected individuals, and uninfected vaccinees saliva was more capable of inhibiting Spike function. Vaccinees with breakthrough Delta infections had Spike-specific IgG levels comparable to those of uninfected vaccinees; however, their ability to inhibit Spike binding was diminished. These data demonstrate that COVID vaccines achieved hoped-for effects in our community, including the generation of mucosal antibodies that inhibit Spike and lower community viral loads, and suggest breakthrough Delta infections were not due to an absence of vaccine-elicited Ig, but instead limited Spike binding activity in the face of high community viral loads.

Heat efficiently inactivates coronaviruses inside vehicles (preprint)

Heat is an established method to inactivate coronaviruses, and there is utility in using heat to reduce viral load on common touch points in vehicles exposed to a person shedding SARS-CoV-2. As SARS-CoV-2 is a Biosafety level (BSL)-3 pathogen, real world testing of heat as a sanitation method for public and private vehicles becomes a challenge, requiring a surrogate coronavirus that can be handled safely outside of a BSL-3 facility. In this study, we used Bovine Coronavirus (BCoV) as a surrogate for SARS-CoV-2 to test the efficacy of heat-based betacoronavirus inactivation. In vitro, a 30-minute exposure to 56{degrees}C completely inactivated BCoV in solution, and a 15-minute exposure reduced recovery of BCoV >1000-fold. When heated to 56{degrees}C for 15 minutes, the infectivity of BCoV spotted and dried on typical porous and non-porous automobile interior materials was reduced by 99 - 99.99%. When BCoV was spotted and dried on hard plastic (seat) material placed inside an out of service transit bus, 56{degrees}C heat for 30 minutes reduced BCoV infectivity 85 - 99.5%. Thus, 56{degrees}C is an accessible, rapid, and effective method to inactivate coronaviruses inside motor vehicles.

A practical PPE decontamination method using warm air and ambient humidity (preprint)

Personal protective equipment (PPE) remains in short supply. Current decontamination methods are complex, slow, expensive and particularly ill-suited for low to middle income nations where the need is greatest. We propose a low temperature, ambient humidity decontamination method (WASP-D) based on the thirty minute or less half-life of Sars-CoV-2 (and other common pathogens) at temperatures above 45C, combined with the observation that most PPE are designed to be safely transported and stored at temperatures below 50C. Decontamination at 12 hours, 46C (115F) and ambient humidity should consistently reduce SARS-CoV-2 viral load by a factor of 10-6, without negatively affecting PPE materials or performance.