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Ravanbakhsh, Reyhaneh, Farhand, Yalda, Ravanbakhsh Ghavghani, Fatemeh. (1403). Investigating the Hepcidin Gene Polymorphisms in COVID-19-Associated Mucormycosis Susceptibility: A Clinical-Laboratory Study. سامانه مدیریت نشریات علمی, 49(7), 450-460. doi: 10.30476/ijms.2023.99589.3167
Reyhaneh Ravanbakhsh; Yalda Farhand; Fatemeh Ravanbakhsh Ghavghani. "Investigating the Hepcidin Gene Polymorphisms in COVID-19-Associated Mucormycosis Susceptibility: A Clinical-Laboratory Study". سامانه مدیریت نشریات علمی, 49, 7, 1403, 450-460. doi: 10.30476/ijms.2023.99589.3167
Ravanbakhsh, Reyhaneh, Farhand, Yalda, Ravanbakhsh Ghavghani, Fatemeh. (1403). 'Investigating the Hepcidin Gene Polymorphisms in COVID-19-Associated Mucormycosis Susceptibility: A Clinical-Laboratory Study', سامانه مدیریت نشریات علمی, 49(7), pp. 450-460. doi: 10.30476/ijms.2023.99589.3167
Ravanbakhsh, Reyhaneh, Farhand, Yalda, Ravanbakhsh Ghavghani, Fatemeh. Investigating the Hepcidin Gene Polymorphisms in COVID-19-Associated Mucormycosis Susceptibility: A Clinical-Laboratory Study. سامانه مدیریت نشریات علمی, 1403; 49(7): 450-460. doi: 10.30476/ijms.2023.99589.3167

Investigating the Hepcidin Gene Polymorphisms in COVID-19-Associated Mucormycosis Susceptibility: A Clinical-Laboratory Study

Iranian Journal of Medical Sciences
مقاله 6، دوره 49، شماره 7، مهر 2024، صفحه 450-460    اصل مقاله (2.54 M)
نوع مقاله: Original Article(s)
شناسه دیجیتال (DOI): 10.30476/ijms.2023.99589.3167
نویسندگان
Reyhaneh Ravanbakhsh1؛ Yalda Farhand2؛ Fatemeh Ravanbakhsh Ghavghani* 2
1Department of Aquatic Biotechnology, Artemia and Aquaculture Research Institute, Urmia University, Urmia, Iran
2Department of Infectious Diseases, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
چکیده
Background: Following the coronavirus disease 2019 outbreak (COVID-19), it became a worrisome health burden worldwide. COVID-19-associated mucormycosis emergence, characterized by dysregulated inflammation and iron metabolism, exacerbated the prognosis of affected patients. Given the significance of hepcidin in regulating inflammation and iron metabolism, this study investigated the significance of hepcidin single nucleotide polymorphisms (SNP) in COVID-19-associated mucormycosis development, along with the association between the clinical and laboratory factors and COVID-19-associated mucormycosis. 
Methods: From September 2021 to November 2021, COVID-19 patients with and without mucormycosis were enrolled in this cross-sectional study. Their medical records and laboratory results were investigated. SNP genotyping was performed using Sanger sequencing. Hardy-Weinberg Equilibrium, Pearson’s Chi square, and student t test were used for analyzing the data using SPSS software version 25. P<0.05 was regarded as statistically significant.
Results: Here, 110 COVID-19 patients with and without mucormycosis were investigated. Elevated levels of urea, aspartate aminotransferase, lactate dehydrogenase, and increased ratio of polymorphonuclear neutrophil to lymphocytes were associated with decreased risk of COVID-19-associated mucormycosis in patients (all P<0.05). Moreover, diabetes mellitus increased the risk of mucormycosis (P=0.028). In contrast to patients without mucormycosis, patients with mucormycosis did not display 442 GA and SNP335 GT genotypes. Unlike patients without mucormycosis, none of the patients with mucormycosis had SNP442 GA and SNP335 GT genotypes. Regarding SNP 443 C>T, and the combination of SNPs 582 A>G and 443 C>T, CC genotype and AA+CC genotypes were associated with increased lactate dehydrogenase levels in COVID-19 patients, respectively. 
Conclusion: Regarding SNP 443 C>T, the CC genotype was associated with increased lactate dehydrogenase levels in COVID-19 patients. In terms of SNP 582 A>G and SNP 443 C>T, COVID-19 patients with AA+CC genotypes had higher levels of LDH. None of the patients with mucormycosis had SNP442 GA and SNP335 GT genotypes.
کلیدواژه‌ها
COVID-19؛ Hepcidin؛ Mucormycosis؛ Polymorphism؛ Single nucleotide
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مراجع
  1. Boni MF, Lemey P, Jiang X, Lam TT, Perry BW, Castoe TA, et al. Evolutionary origins of the SARS-CoV-2 sarbecovirus lineage responsible for the COVID-19 pandemic. Nat Microbiol. 2020;5:1408-17. doi: 10.1038/s41564-020-0771-4. PubMed PMID: 32724171.
  2. Rana R, Tripathi A, Kumar N, Ganguly NK. A Comprehensive Overview on COVID-19: Future Perspectives. Front Cell Infect Microbiol. 2021;11:744903. doi: 10.3389/fcimb.2021.744903. PubMed PMID: 34595136; PubMed Central PMCID: PMCPMC8476999.
  3. Derakhshani A, Hemmat N, Asadzadeh Z, Ghaseminia M, Shadbad MA, Jadideslam G, et al. Arginase 1 (Arg1) as an Up-Regulated Gene in COVID-19 Patients: A Promising Marker in COVID-19 Immunopathy. J Clin Med. 2021;10. doi: 10.3390/jcm10051051. PubMed PMID: 33806290; PubMed Central PMCID: PMCPMC7961773.
  4. Moore JB, June CH. Cytokine release syndrome in severe COVID-19. Science. 2020;368:473-4. doi: 10.1126/science.abb8925. PubMed PMID: 32303591.
  5. Gupta I, Baranwal P, Singh G, Gupta V. Mucormycosis, past and present: a comprehensive review. Future Microbiol. 2023;18:217-34. doi: 10.2217/fmb-2022-0141. PubMed PMID: 36970978.
  6. Sharma R, Kumar P, Rauf A, Chaudhary A, Prajapati PK, Emran TB, et al. Mucormycosis in the COVID-19 Environment: A Multifaceted Complication. Front Cell Infect Microbiol. 2022;12:937481. doi: 10.3389/fcimb.2022.937481. PubMed PMID: 35923801; PubMed Central PMCID: PMCPMC9339637.
  7. Cheng L, Li H, Li L, Liu C, Yan S, Chen H, et al. Ferritin in the coronavirus disease 2019 (COVID-19): A systematic review and meta-analysis. J Clin Lab Anal. 2020;34:e23618. doi: 10.1002/jcla.23618. PubMed PMID: 33078400; PubMed Central PMCID: PMCPMC7595919.
  8. Nemeth E, Ganz T. Hepcidin-Ferroportin Interaction Controls Systemic Iron Homeostasis. Int J Mol Sci. 2021;22. doi: 10.3390/ijms22126493. PubMed PMID: 34204327; PubMed Central PMCID: PMCPMC8235187.
  9. Pagani A, Nai A, Silvestri L, Camaschella C. Hepcidin and Anemia: A Tight Relationship. Front Physiol. 2019;10:1294. doi: 10.3389/fphys.2019.01294. PubMed PMID: 31649559; PubMed Central PMCID: PMCPMC6794341.
  10. Rodriguez R, Jung CL, Gabayan V, Deng JC, Ganz T, Nemeth E, et al. Hepcidin induction by pathogens and pathogen-derived molecules is strongly dependent on interleukin-6. Infect Immun. 2014;82:745-52. doi: 10.1128/IAI.00983-13. PubMed PMID: 24478088; PubMed Central PMCID: PMCPMC3911381.
  11. Ciotti M, Nuccetelli M, Pieri M, Petrangeli CM, Giovannelli A, Cosio T, et al. Evaluation of Hepcidin Level in COVID-19 Patients Admitted to the Intensive Care Unit. Diagnostics (Basel). 2022;12. doi: 10.3390/diagnostics12112665. PubMed PMID: 36359509; PubMed Central PMCID: PMCPMC9689230.
  12. Soliman SSM, El-Labbad EM, Abu-Qiyas A, Fayed B, Hamoda AM, Al-Rawi AM, et al. Novel Secreted Peptides From Rhizopus arrhizus var. delemar With Immunomodulatory Effects That Enhance Fungal Pathogenesis. Front Microbiol. 2022;13:863133. doi: 10.3389/fmicb.2022.863133. PubMed PMID: 35387075; PubMed Central PMCID: PMCPMC8977774.
  13. Hashemi SMA, Thijssen M, Hosseini SY, Tabarraei A, Pourkarim MR, Sarvari J. Human gene polymorphisms and their possible impact on the clinical outcome of SARS-CoV-2 infection. Arch Virol. 2021;166:2089-108. doi: 10.1007/s00705-021-05070-6. PubMed PMID: 33934196; PubMed Central PMCID: PMCPMC8088757.
  14. Chiarella P, Capone P, Sisto R. Contribution of Genetic Polymorphisms in Human Health. Int J Environ Res Public Health. 2023;20. doi: 10.3390/ijerph20020912. PubMed PMID: 36673670; PubMed Central PMCID: PMCPMC9858723.
  15. Liang L, Liu H, Yue J, Liu LR, Han M, Luo LL, et al. Association of Single-Nucleotide Polymorphism in the Hepcidin Promoter Gene with Susceptibility to Extrapulmonary Tuberculosis. Genet Test Mol Biomarkers. 2017;21:351-6. doi: 10.1089/gtmb.2016.0300. PubMed PMID: 28530443.
  16. Stachowska L, Koziarska D, Karakiewicz B, Kotwas A, Knyszynska A, Folwarski M, et al. Hepcidin (rs10421768), Transferrin (rs3811647, rs1049296) and Transferrin Receptor 2 (rs7385804) Gene Polymorphism Might Be Associated with the Origin of Multiple Sclerosis. Int J Environ Res Public Health. 2022;19. doi: 10.3390/ijerph19116875. PubMed PMID: 35682458; PubMed Central PMCID: PMCPMC9180173.
  17. Zarghamian P, Azarkeivan A, Arabkhazaeli A, Mardani A, Shahabi M. Hepcidin gene polymorphisms and iron overload in beta-thalassemia major patients refractory to iron chelating therapy. BMC Med Genet. 2020;21:75. doi: 10.1186/s12881-020-01011-3. PubMed PMID: 32268883; PubMed Central PMCID: PMCPMC7140315.
  18. Wang XY, Yu CX. Research advances on DNA extraction methods from peripheral blood mononuclear cells. Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2014;22:1495-8. doi: 10.7534/j.issn.1009-2137.2014.05.060. PubMed PMID: 25338615.
  19. Balushi AA, Ajmi AA, Sinani QA, Menon V, Berieki ZA, Shezawi AA, et al. COVID-19-Associated Mucormycosis: An Opportunistic Fungal Infection. A Case Series and Review. Int J Infect Dis. 2022;121:203-10. doi: 10.1016/j.ijid.2022.05.005. PubMed PMID: 35533833; PubMed Central PMCID: PMCPMC9075983.
  20. Tabassum T, Araf Y, Moin AT, Rahaman TI, Hosen MJ. COVID-19-associated-mucormycosis: possible role of free iron uptake and immunosuppression. Mol Biol Rep. 2022;49:747-54. doi: 10.1007/s11033-021-06862-4. PubMed PMID: 34709573; PubMed Central PMCID: PMCPMC8552432.
  21. Shirazi F, Kontoyiannis DP, Ibrahim AS. Iron starvation induces apoptosis in Rhizopus oryzae in vitro. Virulence. 2015;6:121-6. doi: 10.1080/21505594.2015.1009732. PubMed PMID: 25830548; PubMed Central PMCID: PMCPMC4601319.
  22. Mahalmani V, Sarma P, Prakash A, Medhi B. Role of Iron Chelators in Mucormycosis. Indian J Pharmacol. 2021;53:261-3. doi: 10.4103/ijp.ijp_604_21. PubMed PMID: 34414902; PubMed Central PMCID: PMCPMC8411966.
  23. Shahcheraghi SH, Hamidfar M, Heidari F, Shahmohammadi S, Akhondimeybodi Z, Fallah T, et al. Evaluation of ESR, CRP, LDH, CPK, D-Dimer, BS and FBS levels in hospitalized COVID-19 patients with mucormycosis. Health Biotechnology and Biopharma (HBB). 2022;6:43-51.
  24. Kumar HM, Sharma P, Rudramurthy SM, Sehgal IS, Prasad KT, Pannu AK, et al. Serum iron indices in COVID-19-associated mucormycosis: A case-control study. Mycoses. 2022;65:120-7. doi: 10.1111/myc.13391. PubMed PMID: 34743358; PubMed Central PMCID: PMCPMC8662179.
  25. Liu J, Sun B, Yin H, Liu S. Hepcidin: A Promising Therapeutic Target for Iron Disorders: A Systematic Review. Medicine (Baltimore). 2016;95:e3150. doi: 10.1097/MD.0000000000003150. PubMed PMID: 27057839; PubMed Central PMCID: PMCPMC4998755.
  26. Hortova-Kohoutkova M, Skotakova M, Onyango IG, Slezakova M, Panovsky R, Opatril L, et al. Hepcidin and ferritin levels as markers of immune cell activation during septic shock, severe COVID-19 and sterile inflammation. Front Immunol. 2023;14:1110540. doi: 10.3389/fimmu.2023.1110540. PubMed PMID: 36776891; PubMed Central PMCID: PMCPMC9911830.
  27. Peng D, Gao Y, Zhang L, Liu Z, Wang H, Liu Y. The Relationship Between Hepcidin-Mediated Iron Dysmetabolism and COVID-19 Severity: A Meta-Analysis. Front Public Health. 2022;10:881412. doi: 10.3389/fpubh.2022.881412. PubMed PMID: 35558525; PubMed Central PMCID: PMCPMC9087037.
  28. Vohra M, Sharma AR, Prabhu BN, Rai PS. SNPs in Sites for DNA Methylation, Transcription Factor Binding, and miRNA Targets Leading to Allele-Specific Gene Expression and Contributing to Complex Disease Risk: A Systematic Review. Public Health Genomics. 2020;23:155-70. doi: 10.1159/000510253. PubMed PMID: 32966991.
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