Comparative aerosol and surface stability of SARS-CoV-2 Variants of Concern

SARS-CoV-2 is transmitted principally via air; contact and fomite transmission may also occur. Variants-of-concern (VOCs) are more transmissible than ancestral SARS-CoV-2. We find that early VOCs show greater aerosol and surface stability than the early WA1 strain, but Delta and Omicron do not. Stability changes do not explain increased transmissibility.

Host and viral determinants of airborne transmission of SARS-CoV-2 in the Syrian hamster

Airborne transmission is one of the major routes contributing to the spread of SARS-CoV-2. Successful aerosol transmission occurs when people release respiratory particles carrying infectious virus in the fine aerosol size range. It remains poorly understood how infection influences the physiological host factors that are integral to this process. Here we assessed the changes in breathing, exhaled droplets, and released virus early after infection with the Alpha and Delta variants in the Syrian hamster. Infection with the two variants led to only nuanced differences in viral tissue titers, disease severity, or shedding magnitude. Both variants led to a short window of detectable virus in the air between 24 h and 48 h, which was poorly reflected by upper respiratory shedding measured in oropharyngeal swabs. The loss of viable air samples coincided with changes in airway constriction as measured by whole body plethysmography, and a decrease of fine aerosols produced in the 1-10 m aerodynamic diameter range. We found that male sex was associated with greater viral replication in the upper respiratory tract and virus shedding in the air. This coincided with an exhaled particle profile shifted towards smaller droplets, independent of variant. Transmission efficiency of Alpha and Delta did not differ on average but exhibited clear variation among donor individuals, including a superspreading event. Transmission leading to substantial dual infections only occurred when both viruses were shed by the same donor and exposure was prolonged. These findings provide direct experimental evidence that quantitative and qualitative assessment of exhaled aerosols may be critical for understanding the limitations and determinants of efficient airborne transmission, thus allowing us to control the pandemic with non-pharmaceutical interventions. SignificanceAirborne transmission is one of the major routes for SARS-CoV-2, however underlying host and virus parameters remain poorly understood. Here, we provide direct experimental evidence that the quantitative and qualitative assessment of exhaled aerosols are critical to understand the efficiency of SARS-CoV-2 airborne transmission. We show that after infection, the Alpha and Delta variants of concern displayed a short window of detectable virus in the air in contrast to prolonged shedding measured in oropharyngeal swabs. The limited window coincided with changes in airway constriction, and a sex dependent decrease of fine aerosols produced in the 1-10 m aerodynamic diameter range. Dual airborne infections only occurred when both viruses were shed by the same donor and after prolonged exposure.

Mitigating outbreaks in congregate settings by decreasing the size of the susceptible population

While many transmission models have been developed for community spread of respiratory pathogens, less attention has been given to modeling the interdependence of disease introduction and spread seen in congregate settings, such as prisons or nursing homes. As demonstrated by the explosive outbreaks of COVID-19 seen in congregate settings, the need for effective outbreak prevention and mitigation strategies for these settings is critical. Here we consider how interventions that decrease the size of the susceptible populations, such as vaccination or depopulation, impact the expected number of infections due to outbreaks. Introduction of disease into the resident population from the community is modeled as a branching process, while spread between residents is modeled via a compartmental model. Control is modeled as a proportional decrease in both the number of susceptible residents and the reproduction number. We find that vaccination or depopulation can have a greater than linear effect on anticipated infections. For example, assuming a reproduction number of 3.0 for density-dependent COVID-19 transmission, we find that reducing the size of the susceptible population by 20% reduced overall disease burden by 47%. We highlight the California state prison system as an example for how these findings provide a quantitative framework for implementing infection control in congregate settings. Additional applications of our modeling framework include optimizing the distribution of residents into independent residential units, and comparison of preemptive versus reactive vaccination strategies.

The effect of temperature and humidity on the stability of SARS-CoV-2 and other enveloped viruses

Environmental conditions affect virus inactivation rate and transmission potential. Understanding those effects is critical for anticipating and mitigating epidemic spread. Ambient temperature and humidity strongly affect the inactivation rate of enveloped viruses, but a mechanistic, quantitative theory of those effects has been elusive. We measure the stability of the enveloped respiratory virus SARS-CoV-2 on an inert surface at nine temperature and humidity conditions and develop a mechanistic model to explain and predict how temperature and humidity alter virus inactivation. We find SARS-CoV-2 survives longest at low temperatures and extreme relative humidities; median estimated virus half-life is over 24 hours at 10 {degrees}C and 40 % RH, but approximately 1.5 hours at 27 {degrees}C and 65 % RH. Our mechanistic model uses simple chemistry to explain the increase in virus inactivation rate with increased temperature and the U-shaped dependence of inactivation rate on relative humidity. The model accurately predicts quantitative measurements from existing studies of five different human coronaviruses (including SARS-CoV-2), suggesting that shared mechanisms may determine environmental stability for many enveloped viruses. Our results indicate scenarios of particular transmission risk, point to pandemic mitigation strategies, and open new frontiers in the mechanistic study of virus transmission.

Quantifying antibody kinetics and RNA shedding during early-phase SARS-CoV-2 infection

Our ability to understand and mitigate the spread of SARS-CoV-2 depends largely on antibody and viral RNA data that provide information about past exposure and shedding. Five months into the outbreak there is an impressive number of studies reporting antibody kinetics and RNA shedding dynamics, but extensive variation in detection assays, study group demographics, and laboratory protocols has presented a challenge for inferring the true biological patterns. Here, we combine existing data on SARS-CoV-2 IgG, IgM and RNA kinetics using a formal quantitative approach that enables integration of 3,214 data points from 516 individuals, published in 22 studies. This allows us to determine the mean values and distributions of IgG and IgM seroconversion times and titer kinetics, and to characterize how antibody and RNA detection probabilities change during the early phase of infection. We observe extensive variation in antibody response patterns and RNA detection patterns, explained by both individual heterogeneity and protocol differences such as targeted antigen and sample type. These results provide a robust reference for clinical management of individual patients, and a foundation for the mathematical models and serological surveys that underpin public health policies.

Estimated effectiveness of traveller screening to prevent international spread of 2019 novel coronavirus (2019-nCoV)

Traveller screening is being used to limit further global spread of 2019 novel coronavirus (nCoV) following its recent emergence. Here, we project the impact of different travel screening programs given remaining uncertainty around the values of key nCoV life history and epidemiological parameters. Even under best-case assumptions, we estimate that screening will miss more than half of infected travellers. Breaking down the factors leading to screening successes and failures, we find that most cases missed by screening are fundamentally undetectable, because they have not yet developed symptoms and are unaware they were exposed. These findings emphasize the need for measures to track travellers who become ill after being missed by a travel screening program. We make our model available for interactive use so stakeholders can explore scenarios of interest using the most up-to-date information. We hope these findings contribute to evidence-based policy to combat the spread of nCoV, and to prospective planning to mitigate future emerging pathogens.