Please use this identifier to cite or link to this item: http://hdl.handle.net/10773/33907
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dc.contributor.authorMarçalo, R.pt_PT
dc.contributor.authorNeto, S.pt_PT
dc.contributor.authorPinheiro, M.pt_PT
dc.contributor.authorRodrigues, A. J.pt_PT
dc.contributor.authorSousa, N.pt_PT
dc.contributor.authorSantos, M. A. S.pt_PT
dc.contributor.authorSimão, P.pt_PT
dc.contributor.authorValente, C.pt_PT
dc.contributor.authorAndrade, L.pt_PT
dc.contributor.authorMarques, A.pt_PT
dc.contributor.authorMoura, G. R.pt_PT
dc.date.accessioned2022-05-17T15:59:55Z-
dc.date.available2022-05-17T15:59:55Z-
dc.date.issued2021-
dc.identifier.urihttp://hdl.handle.net/10773/33907-
dc.description.abstractPeople with chronic obstructive pulmonary disease (COPD) constitute one of COVID-19 risk groups. Variability in predisposition and clinical response to COVID-19 exist but our understanding of these factors in the COPD population is limited. This study explored the genetic background as a possible answer to COVID-19 infection response heterogeneity, either for the poor prognosis in people with COPD or across worldwide populations. Our cohort comprises 255 people with COPD (66±9 years; 72% male; FEV1 53.01±20.31% predicted) and 243 controls (67±10 years; 80% male; FEV1 100.46±19.19% predicted) clinically characterized and genotyped using saliva samples. COVID-19 associated SNPs (susceptibility: rs286914 and rs12329760; and severity: rs657152 and rs11385942) were assessed in our cohort and in the major world populations. Allelic frequencies were used to calculate the probability of having multiple risk alleles. Polygenic risk analysis was also conducted, in our cohort, for the two mentioned phenotypes (susceptibility and severity). No differences in genetic risk for COVID-19 susceptibility or severity were found between people with COPD and the control group (all p-values>0.01), either considering risk alleles individually, allelic combinations or polygenic risk scores. All populations, even those sharing European ancestry (Portuguese, Spanish and Italian), showed significant differences from the European (all p-values<0.0001). Our results indicated a low genetic contribution for COVID-19 infection predisposition or worse outcomes in people with COPD. We quantified also the high genetic heterogeneity across major world populations for the same alleles, even within European subpopulations.pt_PT
dc.language.isoengpt_PT
dc.relationPOCI-01-0145-FEDER-028806pt_PT
dc.relationPOCI-01-0145-FEDER-016428pt_PT
dc.relationCENTRO-01-0246-FEDER-000018pt_PT
dc.relationCENTRO-08-5864-FSE-000039pt_PT
dc.relationinfo:eu-repo/grantAgreement/FCT/9471 - RIDTI/PTDC%2FDTP-PIC%2F2284%2F2014/PTpt_PT
dc.relationinfo:eu-repo/grantAgreement/FCT/9471 - RIDTI/PTDC%2FSAU-SER%2F28806%2F2017/PTpt_PT
dc.relationinfo:eu-repo/grantAgreement/FCT/9471 - RIDTI/PTDC%2FBIA-MIC%2F31849%2F2017/PTpt_PT
dc.relationinfo:eu-repo/grantAgreement/FCT/OE/UI%2FBD%2F151337%2F2021/PTpt_PT
dc.relationinfo:eu-repo/grantAgreement/FCT/6817 - DCRRNI ID/UIDP%2F04501%2F2020/PTpt_PT
dc.rightsopenAccesspt_PT
dc.subjectCOPDpt_PT
dc.subjectCOVID-19pt_PT
dc.subjectGeneticpt_PT
dc.titleDeciphering COPD as a risk group for COVID-19: can we blame genetics?pt_PT
dc.typeconferenceObjectpt_PT
dc.description.versionpublishedpt_PT
dc.peerreviewedyespt_PT
ua.event.date18-19 November, 2021pt_PT
degois.publication.title25th Annual Meeting da Sociedade Portuguesa de Genética Humanapt_PT
Appears in Collections:ESSUA - Comunicações
DCM - Comunicações
IBIMED - Comunicações
Lab3R - Comunicações

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