Duespohl, Matthew W.
(2021)
Investigating Complement Activation in a Cohort of Severely Ill COVID-19 Patients.
Master Essay, University of Pittsburgh.
Abstract
After its emergence in 2019, COVID-19 has quickly become a leading cause of morbidity and mortality in many nations. Furthermore, the emergence of variants of concern has led to fears that SARS-CoV-2, the virus responsible for COVID-19, could begin evading vaccine acquired immunity. Thus, understanding the factors contributing to severe disease progression is critically important to the public health response and the treatment of severely ill COVID-19 patients. This study examines the role complement protein has in development of severe disease in COVID-19 patients. Complement is a group of proteins that play a critical part of the innate immune system responsible for immune cell recruitment, bacterial lysis, and opsonization of pathogens among many things. To examine the role, complement plays in progression of disease severity in COVID-19 patients, a cohort of hospitalized patients was selected from volunteers admitted to the University of Pittsburgh Medical Center Presbyterian Hospital in Allegheny County, Pennsylvania. Serum from the patients was collected as part of routine medical procedures and excess serum was analyzed via ELISA assays to determine the level of complement factor proteins during disease progression. Following analysis, it was clear that complement factor proteins were significantly elevated in patients with higher body mass index scores. Additionally, it was demonstrated that complement factor proteins were positively correlated with the ratio of IgG antibodies and IgA antibodies. Furthermore, it was demonstrated that patients with higher ratios of IgG to IgA, and thus higher complement levels, had more severe disease compared to those with higher ratios of IgA to IgG. Together this suggests that IgA is protective against severe disease by down regulating complement activation, and suggesting higher levels of complement activation was a contributor to more severe disease potentially through inflammatory pathways.
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Details
| Item Type: |
Other Thesis, Dissertation, or Long Paper
(Master Essay)
|
| Status: |
Unpublished |
| Creators/Authors: |
| Creators | Email | Pitt Username | ORCID  |
|---|
| Duespohl, Matthew W. | mwd30@pitt.ed | mwd30 | |
|
| Contributors: |
| Contribution | Contributors Name | Email | Pitt Username | ORCID |
|---|
| Thesis advisor | Marques, Ernesto T.A | marques@pitt.edu | marques | UNSPECIFIED | | Committee Member | Mattila, Joshua T. | jmattila@pitt.edu | jmattila | UNSPECIFIED | | Committee Member | Reed, Douglas S. | dsreed@pitt.edu | dsreed | UNSPECIFIED |
|
| Date: |
31 August 2021 |
| Date Type: |
Completion |
| Submission Date: |
29 August 2021 |
| Access Restriction: |
No restriction; Release the ETD for access worldwide immediately. |
| Number of Pages: |
50 |
| Institution: |
University of Pittsburgh |
| Schools and Programs: |
School of Public Health > Infectious Diseases and Microbiology |
| Degree: |
MPH - Master of Public Health |
| Thesis Type: |
Master Essay |
| Refereed: |
Yes |
| Uncontrolled Keywords: |
COVID-19, SARS-CoV-2, Coronavirus, Complement |
| Date Deposited: |
31 Aug 2021 20:30 |
| Last Modified: |
31 Aug 2021 20:30 |
| URI: |
http://d-scholarship.pitt.edu/id/eprint/41745 |
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