Inactivation of Four Structurally Distinct Respiratory Viruses in Respiratory Droplets at Variable Relative Humidity

NICOLE C. ROCKEY, Duke University

     Abstract Number: 416
     Working Group: Bioaerosols

Abstract
Respiratory infections from viral pathogens cause significant morbidity and mortality each year globally. These viruses transmit to susceptible hosts via numerous routes, including through inhalation or spray of aerosols or droplets emitted by a shedding individual or contact with surfaces contaminated by a shedding individual. Importantly, these transmission routes dictate that respiratory viruses are exposed to the environment in which spread occurs. Sustained virus infectivity during this environmental transport phase is critical for successful spread. Various environmental factors can affect stability during this stage of transmission, including relative humidity (RH), temperature, pH, and aerosol or droplet particle composition. Virus inactivation may result from structural damage or conformational changes to viral proteins, the lipid membrane, and/or the viral genome. Respiratory viruses exhibit a diverse range of virion structures, and these viral attributes also likely impact virus stability. However, the mechanisms driving virus inactivation in indoor spaces, which are often associated with elevated transmission rates, are not well understood; how these mechanisms may differ from virus to virus is also unclear.

Here, we address these knowledge gaps by evaluating the reduction in infectivity of four important but distinct enveloped and nonenveloped human respiratory viruses (i.e., influenza viruses, coronaviruses, rhinoviruses, adenoviruses) in saliva droplets under a range of environmental conditions (e.g., 20% to 80% RH) representative of indoor settings. In parallel, we assess viral protein damage using enzyme-linked immunosorbent assays and genome degradation using quantitative PCR covering a large percentage of each viral genome (i.e., ~50%). Our findings will provide a comprehensive dataset of the relative persistence of prominent human respiratory viruses to better understand settings conducive to environmental virus inactivation. These data are critical to informing engineering treatments targeted at specific pathogens to rapidly decrease infectious viral loads during intervals of elevated community spread.