Toward a Mechanistic Understanding of Inactivation of Respiratory Viruses in the Environment

dc.contributor.authorLongest, Alexandra Kennedyen
dc.contributor.committeechairMarr, Linsey C.en
dc.contributor.committeememberIsaacman-VanWertz, Gabrielen
dc.contributor.committeememberPruden-Bagchi, Amy Jillen
dc.contributor.committeememberLakdawala, Seema S.en
dc.contributor.committeememberVikesland, Peter J.en
dc.contributor.departmentCivil and Environmental Engineeringen
dc.date.accessioned2025-01-04T09:01:20Zen
dc.date.available2025-01-04T09:01:20Zen
dc.date.issued2025-01-03en
dc.description.abstractAirborne transmission of most respiratory viruses was not widely acknowledged until the COVID-19 pandemic. For viruses to transmit between infected and healthy individuals, they must remain stable (i.e., "survive") in aerosols and droplets. Their stability is influenced by many factors including temperature, relative humidity (RH), physico-chemical properties of the carrier droplet, and virus strain. However, the exact mechanisms of viral inactivation remain unknown. The primary aim of this work was to delineate the complex interactions occurring within aerosols and droplets and the mechanisms that drive inactivation of viruses within them. Initially, we reviewed and synthesized existing studies on aerosols and droplets to identify knowledge gaps regarding these mechanisms. This system is highly complex, with various factors influencing viral stability interacting with each other. We recommend that future studies focus on more physiologically relevant aerosol and droplet sizes and fluids to better understand this system in real-world contexts. As previous studies often used large droplets, we shifted our focus to the environmental stability of enveloped viruses (Phi6, influenza virus, and SARS-CoV-2) as a function of initial droplet size (50, 5, and 1 µL) and evaporation kinetics. Our findings indicated that RH had a greater impact on viral decay in large droplets compared to small droplets, and in addition, suggested caution when using surrogates to study the stability of pathogenic viruses. Subsequently, we explored how gas-phase composition and pH affect influenza stability by manipulating the surrounding air. Results indicated that pH has little influence on influenza virus in saliva droplets, implying that another factor may drive decay. Lastly, we examined the survival of influenza virus in the presence of reactive oxygen species (ROS) scavengers, finding that certain ROS may play a significant role in virus inactivation.en
dc.description.abstractgeneralAirborne transmission of most respiratory viruses was not widely acknowledged until the COVID-19 pandemic. For these viruses to spread from one person to another, they must survive in aerosols and droplets. Research has shown that their survival depends on many factors including temperature, humidity, physical and chemical properties of the droplets, and the type of virus. However, we still do not fully understand how viruses decay. The main goal of this work was to understand the complex interactions within aerosols and droplets that lead to virus decay. Initially, we reviewed existing research to find out what we already know and what gaps exist in our knowledge. This is a very complicated system because it involves many factors that can interact with each other. We recommend that future studies use droplet sizes that are more similar to those found in real-world situations and real respiratory fluids, such as saliva. Since many previous studies used droplets that are much larger than what we expel, we determined whether virus survival depends on droplet size and how droplets evaporate. We found that humidity had a greater impact on virus decay in large droplets compared to small droplets. Next, we explored how the air surrounding saliva droplets containing the flu virus affects the virus and the pH of droplets. We found that pH has little effect on flu virus decay, suggesting that another factor may drive decay. Instead, our results indicated that very reactive chemicals may be responsible for virus decay.en
dc.description.degreeDoctor of Philosophyen
dc.format.mediumETDen
dc.identifier.othervt_gsexam:42241en
dc.identifier.urihttps://hdl.handle.net/10919/123902en
dc.language.isoenen
dc.publisherVirginia Techen
dc.rightsIn Copyrighten
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/en
dc.subjectvirusen
dc.subjectviabilityen
dc.subjectdecayen
dc.subjectinactivationen
dc.subjectaerosolsen
dc.subjectdropletsen
dc.subjectinfluenzaen
dc.titleToward a Mechanistic Understanding of Inactivation of Respiratory Viruses in the Environmenten
dc.typeDissertationen
thesis.degree.disciplineCivil Engineeringen
thesis.degree.grantorVirginia Polytechnic Institute and State Universityen
thesis.degree.leveldoctoralen
thesis.degree.nameDoctor of Philosophyen

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