A haemochromatosis-causing HFE mutation is associated with SARS-CoV-2 susceptibility in the Czech population
Jazyk angličtina Země Nizozemsko Médium print-electronic
Typ dokumentu časopisecké články
PubMed
36572138
PubMed Central
PMC9788844
DOI
10.1016/j.cca.2022.12.025
PII: S0009-8981(22)01427-9
Knihovny.cz E-zdroje
- Klíčová slova
- COVID-19, HFE, Iron, Polymorphism, Susceptibility,
- MeSH
- COVID-19 * genetika MeSH
- hemochromatóza * genetika epidemiologie MeSH
- jednonukleotidový polymorfismus MeSH
- lidé MeSH
- MHC antigeny I. třídy genetika MeSH
- mutace MeSH
- protein hemochromatózy genetika MeSH
- SARS-CoV-2 MeSH
- železo MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- Geografické názvy
- Česká republika MeSH
- Názvy látek
- HFE protein, human MeSH Prohlížeč
- MHC antigeny I. třídy MeSH
- protein hemochromatózy MeSH
- železo MeSH
BACKGROUND: Coronavirus disease (COVID-19), which is caused by the SARS-CoV-2 virus, has become a global pandemic. While susceptibility to COVID-19 is subject to several external factors, including hypertension, BMI, and the presence of diabetes, it is also genetically determined to a significant extent. Infectious agents require iron (Fe) for proper functioning. Carriers of mutations resulting in increased iron concentrations are understood to be at increased risk of COVID-19. METHODS: We examined HFE genotypes associated with hereditary haemochromatosis (rs1800562 and rs1799945 SNPs) in 617 COVID-19 patients (166 asymptomatic, 246 symptomatic and 205 hospitalised survivors) and 2 559 population-based controls. RESULTS: We found a higher frequency of the minor allele (Tyr282) of the rs1800562 polymorphism (P < 0.002) in patients compared to controls (8.5 % vs 5.5 %). Non-carriers of the minor allele were protected against SARS-Cov-2 infection (OR, 95 %CI; 0.59, 0.42-0.82). The frequency of minor allele carriers was almost identical across asymptomatic, symptomatic, and hospitalised survivors. The rs1799945 variant did not affect disease severity and its occurrence was almost identical in patients and controls (P between 0.58 and 0.84). CONCLUSIONS: In conclusion, our results indicate that presence of the rs1800562 minor allele, which is associated with hereditary haemochromatosis (thus increased levels of plasma Fe), increases susceptibility to SARS-CoV-2.
Zobrazit více v PubMed
Gorbalenya A.E., Baker S.C., Baric R.S., de Groot R.J., Drosten C., Gulyaeva A.A., Haagmans B.L., Lauber C., Leontovich A.M., Neuman B.W., Penza D., Perlman S., Poon L.L.M., Samborskiy D., Sidorov I.A., Sola I., Ziebuhr J. Severe acute respiratory syndrome-related coronavirus: classifying 2019-nCoV and naming it SARS-CoV-2. Nat. Microbiol. 2020;5:536–544. doi: 10.1038/s41564-020-0695-z. PubMed DOI PMC
K.B. Fowler, S.A. Ross, M. Shimamura, A. Ahmed, A.L. Palmer, M.G. Michaels, D.I. Bernstein, P.J. Sánchez, K.N. Feja, A. Stewart, S. Boppana S. Racial and ethnic differences in the prevalence of congenital cytomegalovirus infection. J. Pediatr. 200 (2018) 196-201.e1, Doi: 10.1016/j.jpeds.2018.04.043. PubMed
Stevenson C.R., Forouhi N.G., Roglic G., Williams B.G., Lauer J.A., Dye C., Unwin N. Diabetes and tuberculosis: the impact of the diabetes epidemic on tuberculosis incidence. BMC Public Health. 2007;7:234. doi: 10.1186/1471-2458-7-234. PubMed DOI PMC
Hippisley-Cox J., Young D., Coupland C., Channon K.M., Tan P.S., Harrison D.A., Rowan K., Aveyard P., Pavord I.D., Watkinson P.J. Risk of severe COVID-19 disease with ACE inhibitors and angiotensin receptor blockers: cohort study including 8.3 million people. Heart. 2020;106:1503–1511. doi: 10.1136/heartjnl-2020-317393. PubMed DOI PMC
Hubacek J.A. Effects of selected inherited factors on susceptibility to SARS-CoV-2 infection and COVID-19 progression. Physiol. Res. 2021;70(S2):S125–S134. doi: 10.33549/physiolres.934730. PubMed DOI PMC
Delanghe J.R., De Buyzere M.L., Speeckaert M.M. Genetic polymorphisms in the host and COVID-19 infection. Adv. Exp. Med. Biol. 2021;1318:109–118. doi: 10.1007/978-3-030-63761-3_7. PubMed DOI
J.R. Delanghe, M.M. Speeckaert Host polymorphisms and COVID-19 infection. Adv. Clin. Chem. 107 (2022) 41-77, Doi: 10.1016/bs.acc.2021.07.002. PubMed PMC
Kaltoum A.B.O. Mutations and polymorphisms in genes involved in the infections by covid 19: a review. Gene Rep. 2021;23 doi: 10.1016/j.genrep.2021.101062. PubMed DOI PMC
Delanghe J.R., Speeckaert M.M., De Buyzere M.L. The host's angiotensin-converting enzyme polymorphism may explain epidemiological findings in COVID-19 infections. Clin. Chim. Acta. 2020;505:192–193. doi: 10.1016/j.cca.2020.03.031. PubMed DOI PMC
T. Ganz. Iron and infection. Int. J. Hematol. 107 (2018) 7-15. Erratum in: Int. J. Hematol. 2017; Dec 2, Doi: 10.1007/s12185-017-2366-2. PubMed
Schmidt S.M. The role of iron in viral infections. Front. Biosci. (Landmark Ed) 2020;25:893–911. doi: 10.2741/4839. PubMed DOI
Edeas M., Saleh J., Peyssonnaux C. Iron: Innocent bystander or vicious culprit in COVID-19 pathogenesis? Int. J. Infect. Dis. 2020;97:303–305. doi: 10.1016/j.ijid.2020.05.110. PubMed DOI PMC
Bastin A., Shiri H., Zanganeh S., Fooladi S., Momeni Moghaddam M.A., Mehrabani M., Nematollahi M.H. Iron chelator or iron supplement consumption in COVID-19? The role of iron with severity infection. Biol. Trace Elem. Res. 2022;200:4571–4581. doi: 10.1007/s12011-021-03048-8. PubMed DOI PMC
Liu W., Zhang S., Nekhai S., Liu S. Depriving iron supply to the virus represents a promising adjuvant therapeutic against viral survival. Curr. Clin. Microbiol. Rep. 2020;7:1–7. doi: 10.1007/s40588-020-00140-w. PubMed DOI PMC
Kawabata H. The mechanisms of systemic iron homeostasis and etiology, diagnosis, and treatment of hereditary hemochromatosis. Int. J. Hematol. 2018;107:31–43. doi: 10.1007/s12185-017-2365-3. PubMed DOI
Beckman L.E., Saha N., Spitsyn V., Van Landeghem G., Beckman L. Ethnic differences in the HFE codon 282 (Cys/Tyr) polymorphism. Hum. Hered. 1997;47:263–267. doi: 10.1159/000154422. PubMed DOI
Merryweather-Clarke A.T., Pointon J.J., Jouanolle A.M., Rochette J., Robson K.J. Geography of HFE C282Y and H63D mutations. Genet. Test. 2000;4:183–198. doi: 10.1089/10906570050114902. PubMed DOI
Heath K.M., Axton J.H., McCullough J.M., Harris N. The evolutionary adaptation of the C282Y mutation to culture and climate during the European Neolithic. Am. J. Phys. Anthropol. 2016;160:86–101. doi: 10.1002/ajpa.22937. PubMed DOI PMC
Adler G., Clark J.S., Łoniewska B., CiechanowiczA A. Prevalence of 845G>A HFE mutation in Slavic populations: an east-west linear gradient in South Slavs. Croat. Med. J. 2011;52:351–357. doi: 10.3325/cmj.2011.52.351. PubMed DOI PMC
Hubacek J.A., Dusek L., Majek O., Adamek V., Cervinkova T., Dlouha D., Pavel J., Adamkova V. CCR5Delta32 deletion as a protective factor in Czech first-wave COVID-19 subjects. Physiol. Res. 2021;70:111–115. doi: 10.33549/physiolres.934647. PubMed DOI PMC
Hubacek J.A., Dusek L., Majek O., Adamek V., Cervinkova T., Dlouha D., Adamkova V. ACE I/D polymorphism in Czech first-wave SARS-CoV-2-positive survivors. Clin. Chim. Acta. 2021;519:206–209. doi: 10.1016/j.cca.2021.04.024. PubMed DOI PMC
Cífková R., Skodová Z., Bruthans J., Adámková V., Jozífová M., Galovcová M., Wohlfahrt P., Krajcoviechová A., Poledne R., Stávek P., Lánská V. Longitudinal trends in major cardiovascular risk factors in the Czech population between 1985 and 2007/8. Czech MONICA and Czech post-MONICA. Atherosclerosis. 2010;211:676–681. doi: 10.1016/j.atherosclerosis.2010.04.007. PubMed DOI
Hubacek J.A., Vrablik M., Dlouha D., Stanek V., Gebauerova M., Adamkova V., Ceska R., Dostálová G., Linhart A., Vitek L., Pitha J. Gene variants at FTO, 9p21, and 2q36.3 are age-independently associated with myocardial infarction in Czech men. Clin. Chim. Acta. 2016;454:119–123. doi: 10.1016/j.cca.2016.01.005. PubMed DOI
Bloudíčková S., Kuthanová L., Hubáček J.A. MIA group. MTHFR and HFE, but not preproghrelin and LBP, polymorphisms as risk factors for all-cause end-stage renal disease development. Folia Biol. (Praha) 2014;60:83–88. PubMed
Miller S.A., Dykes D.D., Polesky H.F. A simple salting out procedure for DNA extraction from human nucleated cells. Nucleic Acids Res. 1988;16:1215. doi: 10.1093/nar/16.3.1215. PubMed DOI PMC
Cimburová M., Půtová I., Provazníková H., Pintérová D., Horák J. S65C and other mutations in the haemochromatosis gene in the Czech population. Folia Biol. (Praha) 2005;51:172–176. PubMed
Mura C., Raguenes O., Férec C. HFE mutations analysis in 711 hemochromatosis probands: evidence for S65C implication in mild form of hemochromatosis. Blood. 1999;93:2502–2505. PubMed
Drakesmith H., Prentice A. Viral infection and iron metabolism. Nat. Rev. Microbiol. 2008;6:541–552. doi: 10.1038/nrmicro1930. PubMed DOI
Hastie C.E., Mackay D.F., Ho F., Celis-Morales C.A., Katikireddi S.V., Niedzwiedz C.L., Jani B.D., Welsh P., Mair F.S., Gray S.R., O'Donnell C.A., Gill J.M., Sattar N., Pell J.P. Vitamin D concentrations and COVID-19 infection in UK Biobank. Diabetes Metab. Syndr. 2020;14:561–565. doi: 10.1016/j.dsx.2020.04.050. PubMed DOI PMC
Magesh S., John D., Li W.T., Li Y., Mattingly-App A., Jain S., Chang E.Y., Ongkeko W.M. Disparities in COVID-19 outcomes by race, ethnicity, and socioeconomic status: A systematic-review and meta-analysis. JAMA Netw. Open. 2021;4:e2134147. PubMed PMC
Acton R.T., Wiener H.W., Barton J.C. Estimates of European American ancestry in African Americans using HFE p. C282Y. Genet. Test. Mol. Biomarkers. 2020;24:578–583. doi: 10.1089/gtmb.2020.0154. PubMed DOI
Lassale C., Gaye B., Hamer M., Gale C.R., Batty G.D. Ethnic disparities in hospitalisation for COVID-19 in England: The role of socioeconomic factors, mental health, and inflammatory and pro-inflammatory factors in a community-based cohort study. Brain Behav. Immun. 2020;88:44–49. doi: 10.1016/j.bbi.2020.05.074. PubMed DOI PMC
Naugler C. Hemochromatosis: a Neolithic adaptation to cereal grain diets. Med. Hypotheses. 2008;70:691–692. doi: 10.1016/j.mehy.2007.06.020. PubMed DOI
Vrablik M., Tichý L., Freiberger T., Blaha V., Satny M., Hubacek J.A. Genetics of familial hypercholesterolemia: New insights. Front. Genet. 2020;11 doi: 10.3389/fgene.2020.574474. PubMed DOI PMC
Sijbrands E.J., Westendorp R.G., Defesche J.C., de Meier P.H., Smelt A.H., Kastelein J.J. Mortality over two centuries in large pedigree with familial hypercholesterolaemia: family tree mortality study. BMJ. 2001;322:1019–1023. doi: 10.1136/bmj.322.7293.1019. PubMed DOI PMC
Arya N., Chakrabrati S., Hegele R.A., Adams P.C. HFE S65C variant is not associated with increased transferrin saturation in voluntary blood donors. Blood Cells Mol. Dis. 1999;25:354–357. doi: 10.1006/bcmd.1999.0264. PubMed DOI
Traore H.N., Meyer D. The effect of iron overload on in vitro HIV-1 infection. J. Clin. Virol. 2004;31(Suppl 1):S92–S98. doi: 10.1016/j.jcv.2004.09.011. PubMed DOI
M.J. Riley, S.R. Hicks, S. Irvine, T.J. Blanchard, E. Britton, H. Shawki, M. Sajid Pervaiz, T.E. Fletcher. Hereditary haemochromatosis, haemophagocytic lymphohistiocytosis and COVID-19. Clin. Infect. Pract. 7 (2020) 100052, Doi: 10.1016/j.clinpr.2020.100052. PubMed PMC
Delanghe J.R., Speeckaert M.M., De Buyzere M.L. ACE Ins/Del genetic polymorphism and epidemiological findings in COVID-19. Clin. Chem. Lab. Med. 2020;58:1129–1130. doi: 10.1515/cclm-2020-0605. PubMed DOI
Delanghe J.R., Speeckaert M.M., De Buyzere M.L. COVID-19 infections are also affected by human ACE1 D/I polymorphism. Clin. Chem. Lab. Med. 2020;58:1125–1126. doi: 10.1515/cclm-2020-0425. PubMed DOI
Yamamoto N., Nishida N., Yamamoto R., Gojobori T., Shimotohno K., Mizokami M., Ariumi Y. Angiotensin-Converting Enzyme (ACE) 1 gene polymorphism and phenotypic expression of COVID-19 symptoms. Genes (Basel) 2021;12:1572. doi: 10.3390/genes12101572. PubMed DOI PMC
Pendu J.L., Breiman A., Rocher J., Dion M., Ruvoën-Clouet N. ABO blood types and COVID-19: Spurious, anecdotal, or truly important relationships? A reasoned review of available data. Viruses. 2021;13:160. doi: 10.3390/v13020160. PubMed DOI PMC
Zhou S., Butler-Laporte G., Nakanishi T., Morrison D.R., Afilalo J., Afilalo M., Laurent L., Pietzner M., Kerrison N., Zhao K., Brunet-Ratnasingham E., Henry D., Kimchi N., Afrasiabi Z., Rezk N., Bouab M., Petitjean L., Guzman C., Xue X., Tselios C., Vulesevic B., Adeleye O., Abdullah T., Almamlouk N., Chen Y., Chassé M., Durand M., Paterson C., Normark J., Frithiof R., Lipcsey M., Hultström M., Greenwood C.M.T., Zeberg H., Langenberg C., Thysell E., Pollak M., Mooser V., Forgetta V., Kaufmann D.E., Richards J.B. A Neanderthal OAS1 isoform protects individuals of European ancestry against COVID-19 susceptibility and severity. Nat. Med. 2021;27:659–667. doi: 10.1038/s41591-021-01281-1. PubMed DOI
Zeberg H., Pääbo S. The major genetic risk factor for severe COVID-19 is inherited from Neanderthals. Nature. 2020;587:610–612. doi: 10.1038/s41586-020-2818-3. PubMed DOI
ABCA3 and LZTFL1 Polymorphisms and Risk of COVID-19 in the Czech Population