اخبار و اعلانات

 آمار

تعداد نشریات286
تعداد نشریات سازمان84
تعداد شماره‌ها2,996
تعداد مقالات33,553
تعداد مشاهده مقاله44,160,095
تعداد دریافت فایل اصل مقاله20,533,760
Abdulateef Abdullah, Zina, Fouad Ali, Layla. (1404). Severity of COVID-19 infection correlation with IL-17 polymorphism. سامانه مدیریت نشریات علمی, 80(2), 425-434. doi: 10.32592/ARI.2025.80.2.425
Zina Abdulateef Abdullah; Layla Fouad Ali. "Severity of COVID-19 infection correlation with IL-17 polymorphism". سامانه مدیریت نشریات علمی, 80, 2, 1404, 425-434. doi: 10.32592/ARI.2025.80.2.425
Abdulateef Abdullah, Zina, Fouad Ali, Layla. (1404). 'Severity of COVID-19 infection correlation with IL-17 polymorphism', سامانه مدیریت نشریات علمی, 80(2), pp. 425-434. doi: 10.32592/ARI.2025.80.2.425
Abdulateef Abdullah, Zina, Fouad Ali, Layla. Severity of COVID-19 infection correlation with IL-17 polymorphism. سامانه مدیریت نشریات علمی, 1404; 80(2): 425-434. doi: 10.32592/ARI.2025.80.2.425

Severity of COVID-19 infection correlation with IL-17 polymorphism

Archives of Razi Institute
مقاله 6، دوره 80، شماره 2، خرداد و تیر 2025، صفحه 425-434    اصل مقاله (543.7 K)
نوع مقاله: Original Articles
شناسه دیجیتال (DOI): 10.32592/ARI.2025.80.2.425
نویسندگان
Zina Abdulateef Abdullah* ؛ Layla Fouad Ali
University of Baghdad, College of Science, Department of Biology, Baghdad, Iraq.
چکیده
Single nucleotide polymorphisms (SNPs) in many studied genes have been related to the severity of COVID-19. This study was carried out to investigate whether the polymorphisms of two SNPs (rs763780 and rs2275913) of the gene polymorphisms for IL-17 are connected to the COVID-19 severity. The effect of these polymorphisms on the levels of IL-17 and the relationship between the level of IL-17 and the severity of COVID-19 were also investigated. RT-PCR was performed to detect SARS-COV-2. Blood samples have been taken for analyses of IL-17 levels by ELISA test and Genomic DNA was extracted for genotyping. Genotyping was performed using Real Time –Polymerase Chain Reaction. The results indicated that the IL-17 level significantly increases in patients compared with control (healthy people) and there is a relationship between the severity of COVID-19 and IL-17 levels (p<0.01) between severity group. Mean ± SE of IL-17 was 67.99 ±2.05 ng/L for the control group, 147.60 ±3.34 for mild or moderate, (218.15 ±6.27) for the severe group and (283.97 ±5.59) for the critical group. And there is no-significant Relationship between SNP80 and IL-17 level (ng/L) with different types of severity and there is no-significant Relationship between SNP13 and IL-17 level (ng/L) with different types of severity (p ≤ 0.05) both of them. The severity of COVID-19 and the prevalence of the AA genotype were shown to be significantly correlated. Nevertheless, rs2275913 A-allele carriers in the patients were shown to be at risk (P = 0.021) comparison with control group, show increase risk in the severe group (p-value= 0.005, p>0.05) and critical group (p-value = 0.023, p>0.05) but no compact between the mild group, There is no relationship (p< 0.05) between the prevalence of the GA genotype and the severity of COVID-19.
کلیدواژه‌ها
RT-PCR؛ SARS-CoV-2؛ intrlukin-17, HRM RT-PCR, SNP
مراجع
  1. Xu C, Luo X, Yu C, Cao S-J. The 2019-nCoV epidemic control strategies and future challenges of building healthy smart cities. SAGE Publications Sage UK: London, England; 2020. p. 639-44.
  2. Chen Y, Liu Q, Guo D. Emerging coronaviruses: genome structure, replication, and pathogenesis. Journal of medical virology. 2020;92(4):418-23.
  3. Hotez PJ, Bottazzi ME, Corry DB. The potential role of Th17 immune responses in coronavirus immunopathology and
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

vaccine-induced immune enhancement. Elsevier; 2020. p. 165-7.

  1. Jin Y, Yang H, Ji W, Wu W, Chen S, Zhang W, et al. Virology, epidemiology, pathogenesis, and control of COVID-19. Viruses. 2020;12(4):372.
  2. De Haan CA, Kuo L, Masters PS, Vennema H, Rottier PJ. Coronavirus particle assembly: primary structure requirements of the membrane protein. Journal of virology. 1998;72(8):6838-50.
  3. Woo PC, Huang Y, Lau SK, Yuen K-Y. Coronavirus genomics and bioinformatics analysis. viruses. 2010;2(8):1804-20.
  4. Covid C, Team R, COVID C, Team R, Chow N, Fleming-Dutra K, et al. Preliminary estimates of the prevalence of selected underlying health conditions among patients with coronavirus disease 2019—United States, February 12–March 28, 2020. Morbidity and Mortality Weekly Report. 2020;69(13):382.
  5. Ghahramani S, Tabrizi R, Lankarani KB, Kashani SMA, Rezaei S, Zeidi N, et al. Laboratory features of severe vs. non-severe COVID-19 patients in Asian populations: a systematic review and meta-analysis. European journal of medical research. 2020;25(1):1-10.
  6. Salehi-Abari I, Khazaeli S, Salehi-Abari F, Salehi-Abari A. Practical guideline for screening the patients with SARS-CoV-2 infection and Persian Gulf criteria for diagnosis of COVID-19. Advances in Infectious Diseases. 2020;10(03):67.
  7. Yang A-P, Liu J-p, Tao W-q, Li H-m. The diagnostic and predictive role of NLR, d-NLR and PLR in COVID-19 patients. International immunopharmacology. 2020;84:106504.
  8. Channappanavar R, Fehr AR, Vijay R, Mack M, Zhao J, Meyerholz DK, et al. Dysregulated type I interferon and inflammatory monocyte-macrophage responses cause lethal pneumonia in SARS-CoV-infected mice. Cell host & microbe. 2016;19(2):181-93.
  9. Chi Y, Ge Y, Wu B, Zhang W, Wu T, Wen T, et al. Serum cytokine and chemokine profile in relation to the severity of coronavirus disease 2019 in China. The Journal of infectious diseases. 2020;222(5):746-54.
  10. Ge Y, Huang M, Yao Y-m. Biology of interleukin-17 and its pathophysiological significance in sepsis. Frontiers in Immunology. 2020;11:1558.
  11. Gaffen SL, Jain R, Garg AV, Cua DJ. The IL-23–IL-17 immune axis: from mechanisms to therapeutic testing. Nature reviews immunology. 2014;14(9):585-600.
  12. Zhou P, Yang X-L, Wang X-G, Hu B, Zhang L, Zhang W, et al. A pneumonia outbreak associated with a new coronavirus of probable bat origin. nature. 2020;579(7798):270-3.
  13. Zhu N, Zhang D, Wang W, Li X, Yang B, Song J, et al. A novel coronavirus from patients with pneumonia in China, 2019. New England journal of medicine. 2020.
  14. Cary N. Statistical analysis system, User's guide. Statistical. Version 9. SAS Inst Inc USA. 2012.
  15. Rodriguez S, Gaunt TR, Day IN. Hardy-Weinberg equilibrium testing of biological ascertainment for Mendelian randomization studies. American journal of epidemiology. 2009;169(4):505-14.
  16. Organization WH. Coronavirus disease 2019 (COVID-19): situation report, 51. 2020.
  17. Benvenuto D, Giovanetti M, Ciccozzi A, Spoto S, Angeletti S, Ciccozzi M. The 2019‐new coronavirus epidemic: evidence for virus evolution. Journal of medical virology. 2020;92(4):455-9.
  18. Girija AS, Shankar EM, Larsson M. Could SARS-CoV-2-induced hyperinflammation magnify the severity of coronavirus disease (CoViD-19) leading to acute respiratory distress syndrome? Frontiers in Immunology. 2020;11:1206.
  19. Tan L, Wang Q, Zhang D, Ding J, Huang Q, Tang Y-Q, et al. Lymphopenia predicts disease severity of COVID-19: a descriptive and predictive study. Signal transduction and targeted therapy. 2020;5(1):1-3.
  20. Bermejo-Martin JF, Almansa R, Menéndez R, Mendez R, Kelvin DJ, Torres A. Lymphopenic community acquired pneumonia as signature of severe COVID-19 infection. Journal of Infection. 2020;80(5):e23-e4.
  21. Qin C, Ziwei MPLZM, Tao SYMY, Ke PCXMP, Shang MMPK. Dysregulation of immune response in patients with COVID-19 in Wuhan, China; Clinical Infectious Diseases; Oxford Academic. Clinical Infectious Diseases. 2020.
  22. Shoenfeld Y. Corona (COVID-19) time musings: our involvement in COVID-19 pathogenesis, diagnosis, treatment and vaccine planning. Autoimmunity reviews. 2020;19(6):102538.
  23. Jamilloux Y, Henry T, Belot A, Viel S, Fauter M, El Jammal T, et al. Should we stimulate or suppress immune responses in COVID-19? Cytokine and anti-cytokine interventions. Autoimmunity reviews. 2020;19(7):102567.
  24. Ye Q, Wang B, Mao J. The pathogenesis and treatment of theCytokine Storm'in COVID-19. Journal of infection. 2020;80(6):607-13.
  25. Hirano T, Murakami M. COVID-19: a new virus, but a familiar receptor and cytokine release syndrome. Immunity. 2020;52(5):731-3.
  26. McGonagle D, Sharif K, O'Regan A, Bridgewood C. The role of cytokines including interleukin-6 in COVID-19 induced pneumonia and macrophage activation syndrome-like disease. Autoimmunity reviews. 2020;19(6):102537.
  27. Träger K, Schütz C, Fischer G, Schröder J, Skrabal C, Liebold A, et al. Cytokine reduction in the setting of an ARDS-associated inflammatory response with multiple organ failure. Case reports in critical care. 2016;2016.
  28. Huang SR, Ma AY, Liu Y, Qu Y. Effects of inflammatory factors including plasma tumor necrosis factor-α in the clinical treatment of acute respiratory distress syndrome. Oncology Letters. 2017;13(6):5016-20.
  29. Ding Q, Liu G-Q, Zeng Y-Y, Zhu J-J, Liu Z-Y, Zhang X, et al. Role of IL-17 in LPS-induced acute lung injury: an in vivo study. Oncotarget. 2017;8(55):93704.
  30. Mikacenic C, Hansen EE, Radella F, Gharib SA, Stapleton RD, Wurfel MM. IL-17A is associated with alveolar inflammation and poor outcomes in acute respiratory distress syndrome. Critical care medicine. 2016;44(3):496.
  31. Hammad A, Mosaad YM, Hammad EM, Elhanbly S, El-Bassiony SR, Al-Harrass MF, et al. Interleukin-17A rs2275913, Interleukin-17F rs763780 and rs2397084 gene polymorphisms as possible risk factors in Juvenile lupus and lupus related nephritis. Autoimmunity. 2016;49(1):31-40.
آمار
تعداد مشاهده مقاله: 28
تعداد دریافت فایل اصل مقاله: 82


counter
سامانه مدیریت نشریات علمی. طراحی و پیاده سازی از سیناوب