In December 2019 in Wuhan, China was confirmed a novel coronavirus SARS-CoV-2 which causes a novel Coronavirus disease 2019, covid-19. It is highly contagious viral disease that has had severe consequences on the global demographics with more than 6 million deaths worldwide and represents the worst global health crisis since the influenza pandemic in 1918. While many infected with SARS-CoV-2 are asymptomatic or develop mild disease, for others, covid-19 have severe impact and can require hospitalization. In some individuals, however, problems appear even after several months of recovering from covid-19. The most common problems are neurological, respiratory system symptoms, palpitations and muscle pain. So far, the actual cause of these problems has not been discovered and those problems are being treated only symptomatically.
Monocytes are one of the three groups of white blood cells and they represent 3-8% of all white blood cells. White blood cells or leukocytes are a diverse group of cells which are responsible for the human immune response. During circulation in the blood circulatory system, monocytes constantly watch for the presence of microorganisms in the body. When the actual inflammation takes place monocytes migrate from blood to an inflammatory site to perform their functions. They serve three main functions in the immune system. These are phagocytosis, antigen presentation and cytokine production.
In this master thesis, we looked for the potential impact of SARS-CoV-2 on the energy metabolism of monocytes. A new measurement method with the Agilent Seahorse XFe24 extracellular flux analyzer enables us to observe the oxygen consumption rate (mitochondrial respiration) and extracellular acidification rate (glycolysis) in real-time. We analyzed 46 individuals who were divided into three groups – healthy controls (n=16), acute covid-19 patients (n=16) and long covid-19 patients (n=14).
Based on our experiments and results we can conclude that SARS-CoV-2 has an impact on the energy metabolism of monocytes. We discovered decreased oxidative phosphorylation in basal conditions and decreased oxygen consumption rate in order to meet the cellular needs for ATP production in stress situations. We conclude that SARS-CoV-2 damaged function and structure of mitochondria in monocytes.
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