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Project Title
HOST GENETIC FACTORS AND SEVERITY OF ANDES HANTAVIRUS INFECTION: A GENOME WIDE ASSOCIATION STUDY
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Principal Investigator
Status
TERMINADO
Start Date
2011

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Publication

Sociodemographic risk factors of hantavirus cardiopulmonary syndrome ^[Factores de riesgo socio-demográficos del síndrome]

2019 , VIAL COX, MARIA CECILIA , Francisca Valdivieso R. , Analía Cuiza V. , Iris Delgado B. , Grazielle Ribeiro E. , Elena Llop R. , Marcela Ferrés G. , REPETTO LISBOA, MARIA GABRIELA , Raúl Riquelme O. , M. Luisa Rioseco Z. , Mario Calvo A. , Gregory Mertz , VIAL CLARO, PABLO AGUSTIN

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Molecular method for the detection of Andes hantavirus infection: validation for clinical diagnostics

2016 , VIAL COX, MARIA CECILIA , Constanza Martinez-Valdebenito , Susana Rios , MARTINEZ ARENAS, JESSICA ISABEL , VIAL CLARO, PABLO AGUSTIN , Marcela Ferres , Juan C. Rivera , Ruth Perez , Francisca Valdivieso

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Deletions in Genes Participating in Innate Immune Response Modify the Clinical Course of Andes Orthohantavirus Infection

2019 , Grazielle Esteves Ribeiro , Luis Edgardo Leon , Ruth Perez , Analia Cuiza , Pablo Agustin Vial , Marcela Ferres , Gregory J. Mertz , VIAL COX, MARIA CECILIA

Andes 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.

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