dc.contributor.author | Efe Iris N. | |
dc.contributor.author | Akman O. | |
dc.contributor.author | Akin D. | |
dc.contributor.author | Atak P.G. | |
dc.contributor.author | Genc A.C. | |
dc.contributor.author | Simsek F. | |
dc.contributor.author | Yildirmak T. | |
dc.date.accessioned | 2024-02-04T13:30:24Z | |
dc.date.available | 2024-02-04T13:30:24Z | |
dc.date.issued | 2023 | |
dc.identifier.issn | 20083645 | |
dc.identifier.uri | https://doi.org/10.5812/jjm-140726 | |
dc.identifier.uri | http://hdl.handle.net/11446/4912 | |
dc.description.abstract | Background: Early immune responses to COVID-19 can help eliminate the virus; therefore, strategies to improve the immune system have become important in disease prevention. Vitamin D plays a crucial role in the immune response to SARS-CoV-2 by increasing the expression of the vitamin D receptor. Objectives: This study investigated the impact of vitamin D deficiency, Fok 1, and Taq 1 Vitamin D Receptor (VDR) gene polymorphisms and comorbidities on the susceptibility to COVID-19. Methods: Fok1 and Taq1 polymorphisms were analyzed using the RT-PCR method, and vitamin D levels were measured using the chemiluminescence method. A total of 200 patients, 100 with COVID-19 and 100 without, provided blood samples for analysis. Results: The COVID-19 positive group had a significantly lower mean vitamin D level of 16.2 ± 11.3 ng/mL compared to the COVID-19 negative control group, 26.7 ± 15.9 ng/mL (P < 0.001). Individuals with a vitamin D level below 18.4 ng/mL had a 2.448 times higher risk of COVID-19 positivity (P < 0.001). There was no significant difference in the Fok1 and Taq1 gene polymorphisms between the two groups. (P = 0.548 and P = 0.098). The COVID-19 positive group had a significantly higher number of comorbid diseases with 40 (40%) compared to the negative group with 10 (10%) participants (P < 0.001). Conclusions: Levels of vitamin D above the cut-off value of 18.4 ng/mL were found to protect against COVID-19, while the presence of comorbid diseases was identified as a risk factor. However, no association was observed between the Fok1 and Taq1 polymorphisms and susceptibility to COVID-19. © 2023, Efe Iris et al. | en_US |
dc.language.iso | eng | en_US |
dc.publisher | Brieflands | en_US |
dc.relation.ispartof | Jundishapur Journal of Microbiology | en_US |
dc.identifier.doi | 10.5812/jjm-140726 | |
dc.rights | info:eu-repo/semantics/openAccess | en_US |
dc.subject | Calcitriol | en_US |
dc.subject | Comorbidity | en_US |
dc.subject | COVID-19 Receptors | en_US |
dc.subject | Genetic Polymorphism | en_US |
dc.subject | Vitamin D Deficiency | en_US |
dc.subject | DNA directed DNA polymerase | en_US |
dc.subject | fok1 polymerase | en_US |
dc.subject | Taq polymerase | en_US |
dc.subject | unclassified drug | en_US |
dc.subject | vitamin D receptor | en_US |
dc.subject | adult | en_US |
dc.subject | Article | en_US |
dc.subject | blood sampling | en_US |
dc.subject | chemiluminescence immunoassay | en_US |
dc.subject | chemiluminescent microparticle immunoassay | en_US |
dc.subject | chemoluminescence | en_US |
dc.subject | controlled study | en_US |
dc.subject | coronavirus disease 2019 | en_US |
dc.subject | DNA extraction | en_US |
dc.subject | DNA polymorphism | en_US |
dc.subject | female | en_US |
dc.subject | gene sequence | en_US |
dc.subject | genetic polymorphism | en_US |
dc.subject | hospitalization | en_US |
dc.subject | human | en_US |
dc.subject | immune response | en_US |
dc.subject | immune system | en_US |
dc.subject | major clinical study | en_US |
dc.subject | male | en_US |
dc.subject | mortality | en_US |
dc.subject | prevalence | en_US |
dc.subject | real time polymerase chain reaction | en_US |
dc.subject | restriction fragment length polymorphism | en_US |
dc.subject | risk factor | en_US |
dc.subject | sensitivity and specificity | en_US |
dc.subject | Severe acute respiratory syndrome coronavirus 2 | en_US |
dc.subject | single nucleotide polymorphism | en_US |
dc.subject | vitamin D deficiency | en_US |
dc.title | Vitamin D Deficiency and Receptor Polymorphisms as Risk Factors for COVID-19 | en_US |
dc.type | article | en_US |
dc.department | DBÜ | en_US |
dc.identifier.issue | 10 | en_US |
dc.identifier.volume | 16 | en_US |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |
dc.department-temp | Efe Iris, N., Department of Infectious Diseases and Clinical Microbiology, Medical Faculty, Demiroglu Bilim University, Istanbul, Turkey; Akman, O., Department of Physiology, Medical Faculty, Demiroglu Bilim University, Istanbul, Turkey; Akin, D., Department of Pharmacology, Medical Faculty, Bahçeşehir University, Istanbul, Turkey; Atak, P.G., Biochemistry Laboratory, Liv Hospital, Istanbul, Turkey; Genc, A.C., Clinical of Internal Medicine, Sakarya Education and Research Hospital, Sakarya, Turkey; Simsek, F., Clinical of Infectious Diseases and Clinical Microbiology, Cemil Taşçıoğlu Hospital, Istanbul, Turkey; Yildirmak, T., Clinical of Infectious Diseases and Clinical Microbiology, Cemil Taşçıoğlu Hospital, Istanbul, Turkey; Demircan, G., Department of Medical Biology and Genetics Esentepe, Medical Faculty, Demiroglu Bilim University, Istanbul, Turkey | en_US |
dc.identifier.scopus | 2-s2.0-85181973601 | en_US |
dc.identifier.wos | WOS:001155836500002 | en_US |
dc.authorscopusid | 36871687600 | |
dc.authorscopusid | 56419689100 | |
dc.authorscopusid | 7006727741 | |
dc.authorscopusid | 54890716400 | |
dc.authorscopusid | 57220604054 | |
dc.authorscopusid | 36115266400 | |
dc.authorscopusid | 6506861686 | |