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Deletions in genes participating in innate immune response modify the clinical course of andes orthohantavirus infection

dc.contributor.authorRibeiro G.E.
dc.contributor.authorLeon L.E.
dc.contributor.authorPerez R.
dc.contributor.authorCuiza A.
dc.contributor.authorVial P.A.
dc.contributor.authorFerres M.
dc.contributor.authorMertz G.J.
dc.contributor.authorVial C.
dc.date.accessioned2020-09-02T22:26:59Z
dc.date.available2020-09-02T22:26:59Z
dc.date.issued2019
dc.identifier10.3390/v11080680
dc.identifier.citation11, 8, -
dc.identifier.issn19994915
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6013
dc.descriptionAndes orthohantavirus (ANDV) is an important human pathogen causing hantavirus cardiopulmonary syndrome (HCPS) with a fatality rate of 30% in Chile. Around 60% of all cases have a severe clinical course, while the others have a mild clinical course. The main goal of this study was to understand if the genetic variation of patients is associated with the clinical course they develop after ANDV infection. For this, the frequency of copy number variants (CNVs, i.e., deletions and duplications) was studied in 195 patients, 88 with mild and 107 with severe HCPS. CNVs were called from intensity data of the Affymetrix Genome-Wide SNP Array 6.0. The analysis of the data was performed with PennCNV, ParseCNV and R softwares; Results: a deletion of 19, 416 bp in the q31.3 region of chromosome 1 is found more frequently in severe patients (p < 0.05). This region contains Complement Factor H Related (CFHR1) and CFHR3 genes, regulators of the complement cascade. A second deletion of 1.81 kb located in the p13 region of chr20 was significantly more frequent in mild patients (p < 0.05). This region contains the SIRPB1 gene, which participates in the innate immune response, more specifically in neutrophil trans-epithelial migration. Both deletions are associated with the clinical course of HCPS, the first being a risk factor and the second being protective. The participation of genes contained in both deletions in ANDV infection pathophysiology deserves further investigation. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.
dc.language.isoen
dc.publisherMDPI AG
dc.subjectANDV
dc.subjectHantavirus
dc.subjectHCPS
dc.subjectcomplement factor H
dc.subjectgenomic DNA
dc.subjectadult
dc.subjectallele
dc.subjectArticle
dc.subjectartificial ventilation
dc.subjectchromosome 1
dc.subjectclinical outcome
dc.subjectcopy number variation
dc.subjectdisease course
dc.subjectdisease severity
dc.subjectDNA extraction
dc.subjectfemale
dc.subjectgene
dc.subjectgene deletion
dc.subjectgene frequency
dc.subjectgene mapping
dc.subjectgenetic variation
dc.subjectgenome-wide association study
dc.subjectgenotype
dc.subjectHantavirus
dc.subjectHantavirus pulmonary syndrome
dc.subjecthuman
dc.subjectimmune response
dc.subjectinnate immunity
dc.subjectmajor clinical study
dc.subjectmale
dc.subjectnonhuman
dc.subjectOrthohantavirus
dc.subjectpathophysiology
dc.subjectrisk factor
dc.subjectRNA virus
dc.subjectSIRPB1 gene
dc.subjecttransendothelial and transepithelial migration
dc.titleDeletions in genes participating in innate immune response modify the clinical course of andes orthohantavirus infection
dc.typeArticle


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