СORONAVIRUS INFECTION WITH AN OBESITY

 Summary. Relevance of the topic: most of the world is obese and there are enough cases of the impact of this pathology on the development of a complicated and severe course of novel coronavirus (COVID-19)
infection.

Purpose of the study: to study literature data on the effect of obesity on the course of novel coronavirus infection.

Objectives: 1. To consider obesity as a factor contributing to the intensification of inflammatory reactions. 2. To study the etiology and pathogenesis of COVID-19 infection. 3. To establish the relationship  between obesity and complications arising from coronavirus infection. 

Results. The most common feature of COVID-19 is severe acute respiratory syndrome caused by progressive lung consolidation. There is a positive correlation between the duration of COVID-19 infection and the degree of  interstitial fibrosis. Extensive pulmonary fibrosis is one of the main causes of  pulmonary consolidation due to the excessive extracellular matrix component produced by activated myofibroblasts [7]. Pulmonary  lipofibroblasts are a special type of adipocytes that contain typical lipid droplets and are close to the second type of alveolar epithelial cells of the pulmonary interstitium. Lipofibroblasts may result from ectopic fat deposition, which plays a vital role in the progression of COVID-19 in these patients. When exposed to various stimulants, such as hyperoxia and  infection of lung lipofibroblasts, a transdifferentiated myogenic phenotype  called myofibroblasts occurs, which causes pulmonary fibrosis [10]. A  significant number of obese patients have impaired glucose metabolism,  which is considered a risk factor and leads to death. SARS infection has been found to cause hyperglycemia in some patients due to dysfunction of the islets of the pancreas as a result of a viral attack. A similar effect occurs after infection with SARS-COV-2. This explains why 52% of those infected with SARS-COV-2 had hyperglycemia. The level of glucose increase in metabolic  disorders in obese patients can be much higher. Hyperglycemia leads to a  number of complications, including osmotic imbalance of fluid and electrolytes, hyperosmolar non-ketonemic coma, worsening skeletal muscle catabolism, impaired wound healing, altered coagulation, and increased  susceptibility to infections [4]. In addition, hyperglycemia impairs the body's immune function. All of this worsens the clinical outcome of COVID-19. Notably, proper blood glucose control reduces mortality in critically ill  patients, highlighting the importance of blood glucose control.

Conclusion.  The relationship between obesity as a factor complicating the course of  SARS-COV-2 infection has been shown. This mainly concerns the  development of a cytokine storm due to the release of IL-1, IL-6, IL-10 by  adipose tissue, as well as TNF-α. It should be noted that obesity affects the occurrence of concomitant metabolic diseases in patients, such as type 2  diabetes mellitus, coronary heart disease, atherosclerosis, etc., leading to acute myocardial infarction, increased thrombus formation and many other serious conditions. In addition, it is difficult for obese patients to provide specialized medical care when connecting to a ventilator, preventing pressure ulcers and attaching a secondary infection. 

1. José Luis Muñoz Carrillo, Jaime Ortega Martín Del Campo, Oscar Gutiérrez Coronado, et al. Adipose Tissue and Inflammation // IntechOpen. 6. 2018. p. 93 – 121. Doi:10.5772/intechopen.74227

2. Prasad Srikakulapu, Coleen A. McNamara. B Lymphocytes and Adipose Tissue Inflammation//Arteriosclerosis, Thrombosis, and Vascular Biology. 40 (5) . 2020. p. 1110–1122. Doi: 10.1161/ATVBAHA.119.312467

3. Charles Caër, Christine Rouault, Tiphaine Le Roy, et al. Immune cell-derived cytokines contribute to obesity-related inflammation, fibrogenesis and metabolic deregulation in human adipose tissue. 7 (1). 2017. p. 1 – 11. Doi: 10.1038/s41598-017-02660-w

4. Kassem Makki, Philippe Froguel, Isabelle Wolowczuk. Adipose Tissue in Obesity-Related Inflammation and Insulin Resistance: Cells, Cytokines, and Chemokines // ISRN Inflamm. 2013. p.139-239. doi: 10.1155/2013/139239

5. Parisi V, Petraglia L, Cabaro S, et al. Imbalance Between Interleukin-1β and Interleukin-1 Receptor Antagonist in Epicardial Adipose Tissue Is Associated With Non ST-Segment Elevation Acute Coronary Syndrome // Front. Physiol. 11(42).2020. 42p. doi: 10.3389/fphys.2020.00042

6. Elaheh Kordzadeh-Kermani, Hossein Khalili, Iman Karimzadeh. Pathogenesis, clinical manifestations and complications of coronavirus disease 2019 (COVID-19) // FUTURE MICROBIOLOGYVOL. 15(13). 2020. doi: 10.2217/fmb-2020-0110

7. Shintaro Hojyo,Mona Uchida,Kumiko Tanaka, et al. How COVID-19 induces cytokine storm with high mortality // Inflamm Regen. 40. 2020. 37p. doi: 10.1186/s41232-020-00146-3

8. Ragab Dina, Salah Eldin Haitham, Taeimah Mohamed, Khattab Rasha, et al. The COVID-19 Cytokine Storm; What We Know So Far // Frontiers in Immunology. 11. 2020. p. 1446. doi:10.3389/fimmu.2020.01446

9. Kim JS, Lee JY, Yang JW, et al. Immunopathogenesis and treatment of cytokine storm in COVID-19 // Theranostics. 11(1).2021. p.316-329. doi:10.7150/thno.49713.

10. Zhu X, Yang L, Huang K. COVID-19 and Obesity: Epidemiology, Pathogenesis and Treatment. //Diabetes Metab Syndr Obes. 13. 2020. p.4953-4959. doi: 10.2147/DMSO.S285197