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Investigating the Hepcidin Gene Polymorphisms in COVID-19-Associated Mucormycosis Susceptibility: A
Reyhaneh Ravanbakhsh1, Yalda Farhand2, Fatemeh Ravanbakhsh Ghavghani2
1Department of Aquatic Biotechnology, Artemia and Aquaculture Research Institute, Urmia University, Urmia, Iran.
Insights
This study found that certain hepcidin single nucleotide polymorphisms (SNP) were not present in COVID-19 patients with mucormycosis. These findings suggest a potential role for hepcidin SNPs in COVID-19-associated mucormycosis risk.
Area of Science:
- * Medical Science
- * Genetics
- * Infectious Diseases
Background:
- * Coronavirus disease 2019 (COVID-19) poses a significant global health threat.
- * COVID-19-associated mucormycosis, linked to inflammation and iron dysregulation, worsens patient outcomes.
- * Hepcidin plays a crucial role in managing inflammation and iron metabolism.
Purpose of the Study:
- * To investigate the role of hepcidin single nucleotide polymorphisms (SNP) in the development of COVID-19-associated mucormycosis.
- * To explore associations between clinical and laboratory factors and COVID-19-associated mucormycosis.
Main Methods:
- * A cross-sectional study involving 110 COVID-19 patients (with and without mucormycosis) from September to November 2021.
- * SNP genotyping was conducted using Sanger sequencing.
- * Data analysis included Hardy-Weinberg Equilibrium, Pearson's Chi square, and student t-tests (SPSS v25).
Main Results:
- * Elevated urea, AST, LDH, and a higher neutrophil-to-lymphocyte ratio correlated with a decreased risk of mucormycosis.
- * Diabetes mellitus was identified as a risk factor for mucormycosis (P=0.028).
- * Patients with mucormycosis lacked specific genotypes (442 GA, SNP335 GT).
Conclusions:
- * Specific hepcidin genotypes (442 GA, SNP335 GT) were absent in COVID-19 patients with mucormycosis.
- * The CC genotype for SNP 443 C>T and AA+CC genotypes for combined SNPs 582 A>G and 443 C>T were linked to increased lactate dehydrogenase levels.
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.
