Since late 2019 a new coronavirus, SARS-CoV2, has spread through the world and caused a pandemic. The virus causes the heterogenous disease Covid-19, causing flu- like symptoms for most people but can cause Acute Respiratory Distress Syndrome and fatal outcome in some patients. The mechanism is not clearly understood, but depletion of the immunological response has been seen in patients with severe Covid-19. This study will focus on T- lymphocyte, T- cell subtypes, B- lymphocyte, NK- cell and intracytoplasmic interleukin subsets in hospitalized Covid-19 patients to examine immune phenotypes that could be related to, or cause, more severe disease. The method used is multicolour flow cytometry on whole blood and frozen PBMC. Comparison of fraction of each cell type from total cell count, with regard of underlying diseases, age, sex and other factors were done using multivariate regression analysis to evaluate mechanisms correlated to severe disease. The results showed overall lower lymphocyte counts in Covid- patients versus healthy controls. Lower lymphocyte counts were also observed in men versus women. Lower levels of NK-cells and B-cells were found in people in ages over 60 years. Higher glucose levels were associated with lower B-cell and T-regulatory cell counts, while diabetes patients showed higher T-regulatory cell counts. No differences in proinflammatory cytokines were found between patient groups but were slightly higher in patients versus healthy controls. The conclusion of this study is that dysfunction of the immune system caused by infection of SARS-CoV2 gives lymphocytopenia and more severe outcome.
| Identifer | oai:union.ndltd.org:UPSALLA1/oai:DiVA.org:uu-456991 |
| Date | January 2021 |
| Creators | Vredin, Tuva |
| Publisher | Uppsala universitet, Institutionen för medicinsk cellbiologi |
| Source Sets | DiVA Archive at Upsalla University |
| Language | Swedish |
| Detected Language | English |
| Type | Student thesis, info:eu-repo/semantics/bachelorThesis, text |
| Format | application/pdf |
| Rights | info:eu-repo/semantics/openAccess |
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