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Infect Genet Evol. 2016 Oct;44:403-411. doi: 10.1016/j.meegid.2016.07.044. Epub 2016 Aug 2.

Strong down-regulation of glycophorin genes: A host defense mechanism against rotavirus infection.

Author information

1
Unidade de Xenética, Departamento de Anatomía Patolóxica e Ciencias Forenses, Instituto de Ciencias Forenses, Facultade de Medicina, Universidade de Santiago de Compostela, and GENPOB Research Group, Instituto de Investigaciones Sanitarias (IDIS), Hospital Clínico Universitario de Santiago, Galicia, Spain; Grupo de Investigación en Genética, Vacunas, Infecciones y Pediatría (GENVIP), Hospital Clínico Universitario, Universidade de Santiago de Compostela (USC), Galicia, Spain,. Electronic address: antonio.salas@usc.es.
2
Sistemas Genómicos, Paterna, Valencia, Spain.
3
Unidade de Xenética, Departamento de Anatomía Patolóxica e Ciencias Forenses, Instituto de Ciencias Forenses, Facultade de Medicina, Universidade de Santiago de Compostela, and GENPOB Research Group, Instituto de Investigaciones Sanitarias (IDIS), Hospital Clínico Universitario de Santiago, Galicia, Spain; Grupo de Investigación en Genética, Vacunas, Infecciones y Pediatría (GENVIP), Hospital Clínico Universitario, Universidade de Santiago de Compostela (USC), Galicia, Spain.
4
Grupo de Investigación en Genética, Vacunas, Infecciones y Pediatría (GENVIP), Hospital Clínico Universitario, Universidade de Santiago de Compostela (USC), Galicia, Spain.
5
Grupo de Investigación en Genética, Vacunas, Infecciones y Pediatría (GENVIP), Hospital Clínico Universitario, Universidade de Santiago de Compostela (USC), Galicia, Spain,; Translational Pediatrics and Infectious Diseases, Department of Pediatrics, Hospital Clínico Universitario de Santiago de Compostela, Galicia, Spain.

Abstract

The mechanisms of rotavirus (RV) infection have been analyzed from different angles but the way in which RV modifies the transcriptome of the host is still unknown. Whole transcriptome shotgun sequencing of peripheral blood samples was used to reveal patterns of expression from the genome of RV-infected patients. RV provokes global changes in the transcriptome of infected cells, involving an over-expression of genes involved in cell cycle and chromatin condensation. While interferon IFI27 was hyper-activated, interferon type II was not suggesting that RV has developed mechanisms to evade the innate response by host cells after virus infection. Most interesting was the inhibition of genes of the glycophorins A and B (GYPA/B) family, which are the major sialoglycoproteins of the human erythrocyte membrane and receptor of several viruses for host invasion. RV infection induces a complex and global response in the host. The strong inhibition of glycophorins suggests a novel defense mechanism of the host to prevent viral infection, inhibiting the expression of receptors used by the virus for infection. The present results add further support to the systemic nature of RV infection.

KEYWORDS:

Cell cycle; Glycophorin; RNA-Seq; Rotavirus; Transcriptome

PMID:
27491455
DOI:
10.1016/j.meegid.2016.07.044
[Indexed for MEDLINE]

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