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Inoculum Dose and Sepsis Comorbidity...
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Silva, Elvia Elizabeth.
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Inoculum Dose and Sepsis Comorbidity Alter Disease Outcomes in an MHV-1 Murine Model of Beta-Coronavirus Infections.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Inoculum Dose and Sepsis Comorbidity Alter Disease Outcomes in an MHV-1 Murine Model of Beta-Coronavirus Infections./
作者:
Silva, Elvia Elizabeth.
出版者:
Ann Arbor : ProQuest Dissertations & Theses, : 2024,
面頁冊數:
152 p.
附註:
Source: Dissertations Abstracts International, Volume: 86-01, Section: B.
Contained By:
Dissertations Abstracts International86-01B.
標題:
Immunology. -
電子資源:
https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=31148610
ISBN:
9798383188279
Inoculum Dose and Sepsis Comorbidity Alter Disease Outcomes in an MHV-1 Murine Model of Beta-Coronavirus Infections.
Silva, Elvia Elizabeth.
Inoculum Dose and Sepsis Comorbidity Alter Disease Outcomes in an MHV-1 Murine Model of Beta-Coronavirus Infections.
- Ann Arbor : ProQuest Dissertations & Theses, 2024 - 152 p.
Source: Dissertations Abstracts International, Volume: 86-01, Section: B.
Thesis (Ph.D.)--The University of Iowa, 2024.
Immune responses against respiratory viruses have been studied in mouse models for decades, providing insight into the players involved in protection. However, it is also known that patients in the clinic can come in with different comorbidities which make infection worse. Additionally, although exposure length has been studied in the SARS-CoV-2 context, whether the immune response differs when initially exposed to different amounts of coronavirus, has been understudied. In this work I address how sepsis, an immune disorder, and the initial infection amount determine the outcome in beta-coronavirus infection using the MHV-1 mouse model.I noted that in a host whose genetics already predisposes them to severe infection with beta coronavirus, there is a tipping point of asymptomatic to symptomatic and severe infection depending on how much initial virus they receive. This is a different assessment than what is tested in the lungs several days in, which can be much more similar between inoculum doses. A low dose infection was asymptomatic in coronavirus-susceptible mice. While mice had active virus in their lungs and their adaptive immune was responding, they did not experience any outward symptoms and all of them survived. This low dose infection also worked to protect these mice from severe infection later. Specifically, the antibodies generated from the asymptomatic infection protected these mice from a lethal infection. All mice survived and had no detectible virus early after infection.Finally, I addressed the clinically relevant model of prior sepsis as a beta coronavirus infection comorbidity. Hosts who were otherwise resistant to infection due to genetics or initial infection level were worse off if they experienced sepsis before, including poorer morbidity and higher viral load. This thesis covers the alterations in pathology and immune responses after these infection alterations and closes with future directions in immune memory after sepsis.
ISBN: 9798383188279Subjects--Topical Terms:
611031
Immunology.
Subjects--Index Terms:
Coronavirus
Inoculum Dose and Sepsis Comorbidity Alter Disease Outcomes in an MHV-1 Murine Model of Beta-Coronavirus Infections.
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Immune responses against respiratory viruses have been studied in mouse models for decades, providing insight into the players involved in protection. However, it is also known that patients in the clinic can come in with different comorbidities which make infection worse. Additionally, although exposure length has been studied in the SARS-CoV-2 context, whether the immune response differs when initially exposed to different amounts of coronavirus, has been understudied. In this work I address how sepsis, an immune disorder, and the initial infection amount determine the outcome in beta-coronavirus infection using the MHV-1 mouse model.I noted that in a host whose genetics already predisposes them to severe infection with beta coronavirus, there is a tipping point of asymptomatic to symptomatic and severe infection depending on how much initial virus they receive. This is a different assessment than what is tested in the lungs several days in, which can be much more similar between inoculum doses. A low dose infection was asymptomatic in coronavirus-susceptible mice. While mice had active virus in their lungs and their adaptive immune was responding, they did not experience any outward symptoms and all of them survived. This low dose infection also worked to protect these mice from severe infection later. Specifically, the antibodies generated from the asymptomatic infection protected these mice from a lethal infection. All mice survived and had no detectible virus early after infection.Finally, I addressed the clinically relevant model of prior sepsis as a beta coronavirus infection comorbidity. Hosts who were otherwise resistant to infection due to genetics or initial infection level were worse off if they experienced sepsis before, including poorer morbidity and higher viral load. This thesis covers the alterations in pathology and immune responses after these infection alterations and closes with future directions in immune memory after sepsis.
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