Possible effect of OAS1 and TMPRSS6 but not DPP4 and ZNF335 polymorphisms on COVID-19 severity in the Czech population
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články
PubMed
38309700
DOI
10.21101/cejph.a7906
Knihovny.cz E-zdroje
- Klíčová slova
- COVID-19, DPP4, OAS1, SARS-CoV-2, TMPRSS6, ZNF335, polymorphism, severity,
- MeSH
- 2',5'-oligoadenylátsynthetasa MeSH
- COVID-19 * genetika MeSH
- dipeptidylpeptidasa 4 MeSH
- DNA vazebné proteiny MeSH
- jednonukleotidový polymorfismus MeSH
- lidé MeSH
- membránové proteiny MeSH
- SARS-CoV-2 MeSH
- serinové endopeptidasy genetika MeSH
- transkripční faktory MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- Geografické názvy
- Česká republika epidemiologie MeSH
- Názvy látek
- 2',5'-oligoadenylátsynthetasa MeSH
- dipeptidylpeptidasa 4 MeSH
- DNA vazebné proteiny MeSH
- DPP4 protein, human MeSH Prohlížeč
- membránové proteiny MeSH
- OAS1 protein, human MeSH Prohlížeč
- serinové endopeptidasy MeSH
- TMPRSS6 protein, human MeSH Prohlížeč
- transkripční faktory MeSH
- ZNF335 protein, human MeSH Prohlížeč
OBJECTIVES: The acute respiratory syndrome, known as COVID-19, is characterised by high morbidity and increased mortality. Genetic factors may partially explain the differences in susceptibility to and severity of COVID-19. METHODS: We have analysed common functional polymorphisms within the OAS1 (rs4767027), TMPRSS6 (rs855791), DPP4 (rs3788979), and ZNF335 (rs3848719) genes in SARS-CoV-2 positive subjects (n = 521, different disease severity) and in population controls (n = 2,559 subjects, COVID-19 status unknown). RESULTS: Neither DPP4 nor ZNF335 were associated with disease susceptibility or severity in the Czech population in any of the models used for calculation. T allele carriers of the OAS1 polymorphism seem to be protective against symptomatic COVID-19 (p = 0.002 calculated for trend; asymptomatic, symptomatic, hospitalised). Similarly, within the TMPRSS6, minor TT homozygotes associated with lower plasma Fe concentrations were underrepresented in the overall patient group (p = 0.044; OR = 0.77, 95% CI: 0.59-0.99), and the difference was mainly driven by the severe COVID-19 subjects. In general, risky homozygotes of these two polymorphisms were less frequent than expected in the group of hospitalised COVID-19 survivors. CONCLUSIONS: Common variants within OAS1 (rs4767027) and TMPRSS6 (rs855791) play some role in COVID-19 pathology in the Czech Caucasian population. Whether the depletion of minor allele carriers of these two variants is associated with increased COVID-19 mortality, needs to be analysed in an external confirmatory study.
Experimental Medicine Centre Institute for Clinical and Experimental Medicine Prague Czech Republic
Institute of Biostatistics and Analyses Faculty of Medicine Masaryk University Brno Czech Republic
Institute of Health Information and Statistics of the Czech Republic Prague Czech Republic
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Tuček M. COVID-19 in the Czech Republic 2020: probable transmission of the coronavirus SARS-CoV-2. Cent Eur J Public Health. 2021;29(2):159-61. DOI
Komenda M, Jarkovský J, Klimeš D, Panoška P, Šanca O, Gregor J, et al. Sharing datasets of the COVID-19 epidemic in the Czech Republic. PLoS One. 2022;17(4):e0267397. doi: 10.1371/journal.pone.0267397. DOI
Hippisley-Cox J, Young D, Coupland C, Channon KM, Tan PS, Harrison DA, et al. Risk of severe COVID-19 disease with ACE inhibitors and angiotensin receptor blockers: cohort study including 8.3 million people. Heart. 2020;106(19):1503-11. DOI
Zsichla L, Müller V. Risk factors of severe COVID-19: a review of host, viral and environmental factors. Viruses. 2023;15(1):175. doi: 10.3390/v15010175. DOI
Schmidt A, Groh AM, Frick JS, Vehreschild MJGT, Ludwig KU. Genetic predisposition and the variable course of infectious diseases. Dtsch Arztebl Int. 2022;119(8):117-23. DOI
Vannberg FO, Chapman SJ, Hill AV. Human genetic susceptibility to intracellular pathogens. Immunol Rev. 2011;240(1):105-16. DOI
Paces J, Strizova Z, Smrz D, Cerny J. COVID-19 and the immune system. Physiol Res. 2020;69(3):379-88.
Hubacek JA. Effects of selected inherited factors on susceptibility to SARS-CoV-2 infection and COVID-19 progression. Physiol Res. 2021;70(S2):S125-34. DOI
Delanghe JR, Speeckaert MM. Host polymorphisms and COVID-19 infection. Adv Clin Chem. 2022;107:41-77. DOI
Colona VL, Vasiliou V, Watt J, Novelli G, Reichardt JKV. Update on human genetic susceptibility to COVID-19: susceptibility to virus and response. Hum Genomics 2021;15(1):57. doi: 10.1186/s40246-021-00356-x. DOI
Edeas M, Saleh J, Peyssonnaux C. Iron: innocent bystander or vicious culprit in COVID-19 pathogenesis? Int J Infect Dis. 2020;97:303-5. DOI
Delanghe JR, De Buyzere ML, Speeckaert MM. Genetic polymorphisms in the host and COVID-19 infection. Adv Exp Med Biol. 2021;1318:109-18. DOI
Hubacek JA, Philipp T, Adamkova V, Majek O, Dusek L. A haemochromatosis-causing HFE mutation is associated with SARS-CoV-2 susceptibility in the Czech population. Clin Chim Acta. 2023;538:211-5. DOI
Lee P. Role of matriptase-2 (TMPRSS6) in iron metabolism. Acta Haematol. 2009;122(2-3):87-96. DOI
Galesloot TE, Geurts-Moespot AJ, den Heijer M, Sweep FC, Fleming RE, Kiemeney LA, et al. Associations of common variants in HFE and TMPRSS6 with iron parameters are independent of serum hepcidin in a general population: a replication study. J Med Genet. 2013;50(9):593-8. DOI
Esposito S, D'Abrosca G, Antolak A, Pedone PV, Isernia C, Malgieri G. Host and viral zinc-finger proteins in COVID-19. Int J Mol Sci. 2022;23(7):3711. doi: 10.3390/ijms23073711. DOI
Qin S, Xu W, Wang C, Jiang S, Dai W, Yang Y, et al. Analyzing master regulators and scRNA-seq of COVID-19 patients reveals an underlying anti-SARS-CoV-2 mechanism of ZNF proteins. Brief Bioinform. 2021;22(5):bbab118. doi: 10.1093/bib/bbab118. DOI
Shortt K, Chaudhary S, Grigoryev D, Heruth DP, Venkitachalam L, Zhang LQ, et al. Identification of novel single nucleotide polymorphisms associated with acute respiratory distress syndrome by exome-seq. PLoS One. 2014;9(11):e111953. doi: 10.1371/journal.pone.0111953. DOI
Solerte SB, Di Sabatino A, Galli M, Fiorina P. Dipeptidyl peptidase-4 (DPP4) inhibition in COVID-19. Acta Diabetol. 2020;57(7):779-83. DOI
Sebastián-Martín A, Sánchez BG, Mora-Rodríguez JM, Bort A, Díaz-Laviada I. Role of dipeptidyl peptidase-4 (DPP4) on COVID-19 physiopathology. Biomedicines. 2022;10(8):2026. doi: 10.3390/biomedicines10082026. DOI
Posadas-Sánchez R, Sánchez-Muñoz F, Guzmán-Martín CA, Hernández-Díaz Couder A, Rojas-Velasco G, Fragoso JM, et al. Dipeptidylpeptidase-4 levels and DPP4 gene polymorphisms in patients with COVID-19. Association with disease and with severity. Life Sci. 2021;276:119410. doi: 10.1016/j.lfs.2021.119410. DOI
Zeberg H, Pääbo S. The major genetic risk factor for severe COVID-19 is inherited from Neanderthals. Nature. 2020;587:610-2. DOI
Zhou S, Butler-Laporte G, Nakanishi T, Morrison DR, Afilalo J, Afilalo M, et al. A Neanderthal OAS1 isoform protects individuals of European ancestry against COVID-19 susceptibility and severity. Nat Med. 2020;27(7835):659-67. DOI
Hubacek JA, Dusek L, Majek O, Adamek V, Cervinkova T, Dlouha D, et al. CCR5Delta32 deletion as a protective factor in Czech first-wave COVID-19 subjects. Physiol Res. 2021;70(1):111-5.
Hubacek JA, Dusek L, Majek O, Adamek V, Cervinkova T, Dlouha D, et al. ACE I/D polymorphism in Czech first-wave SARS-CoV-2-positive survivors. Clin Chim Acta. 2021;519:206-9. DOI
Hubacek JA, Philipp T, Adamkova V, Majek O, Dusek L. ABCA3 and LZTFL1 polymorphisms and risk of COVID-19 in the Czech Population. Physiol Res. 2023;72(4):539-43. DOI
Cífková R, Skodová Z, Bruthans J, Adámková V, Jozífová M, Galovcová M, et al. Longitudinal trends in major cardiovascular risk factors in the Czech population between 1985 and 2007/8. Czech MONICA and Czech post-MONICA. Atherosclerosis. 2010;211(2):676-81. DOI
Hubácek JA, Adámková V, Ceska R, Poledne R, Horínek A, Vráblík M. New variants in the apolipoprotein AV gene in individuals with extreme triglyceride levels. Physiol Res. 2004;53(2):225-8. DOI
Gokul A, Arumugam T, Ramsuran V. Genetic ethnic differences in human 2'-5'-oligoadenylate synthetase and disease associations: a systematic review. Genes (Basel). 2023;14(2):527. doi: 10.3390/genes14020527. DOI
COVID-19 Host Genetics Initiative. Mapping the human genetic architecture of COVID-19. Nature. 2021;600(7889):472-7.