Global impact of heparin on gene expression profiles in neural cells infected by Enterovirus 71

Journal article


Pourianfar, H. R., Palombo, E. and Grollo, L.. (2014). Global impact of heparin on gene expression profiles in neural cells infected by Enterovirus 71. Intervirology: international journal of basic and medical virology. 57(2), pp. 93 - 100. https://doi.org/10.1159/000355872
AuthorsPourianfar, H. R., Palombo, E. and Grollo, L.
Abstract

Objectives: Heparan sulphate mimetics, particularly heparin (Hep), have previously been shown to considerably inhibit infection of enterovirus 71 (EV71) in Vero cells. Therefore, in this study, a genome-wide DNA microarray was performed to gain insight into the mechanism(s) of action of Hep against infection of a human neural cell line, SK-N-SH, with a clinical strain of EV71. Methods: This study focused on a selection of EV71-induced genes whose expression profiling was exclusively affected by the antiviral activity of Hep. The selection procedure was performed through a statistical multi-level comparison with the following controls: negative control cells, compound control (cells treated with Hep only), virus control (cells treated with virus only) and treatment control (EV71-infected cells treated with Hep). Results: Overall, of more than 30,000 genes studied, 14 well-known annotated genes were selected that may be targets for the antiviral activity of Hep against EV71 infection in neural cells. For most of these genes, Hep appeared to modulate the impact of EV71 infection on the expression pattern of the genes. Conclusions: The findings of this research may provide initial assistance in new directions for studies to design molecular drug targets against EV71 infection.

Year2014
JournalIntervirology: international journal of basic and medical virology
Journal citation57 (2), pp. 93 - 100
ISSN0300-5526
Digital Object Identifier (DOI)https://doi.org/10.1159/000355872
Page range93 - 100
Research GroupSchool of Behavioural and Health Sciences
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File Access Level
Controlled
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