Abstract
Hand, Foot and Mouth Disease (HFMD) is a self-limiting viral disease that mainly affects infants and children. In contrast with other HFMD causing enteroviruses, Enterovirus71 (EV71) has commonly been associated with severe clinical manifestation leading to death. Currently, due to a lack in understanding of EV71 pathogenesis, there is no antiviral therapeutics for the treatment of HFMD patients. Therefore the need to better understand the mechanism of EV71 pathogenesis is warranted. We have previously reported a human colorectal adenocarcinoma cell line (HT29) based model to study the pathogenesis of EV71. Using this system, we showed that knockdown of DGCR8, an essential cofactor for microRNAs biogenesis resulted in a reduction of EV71 replication. We also demonstrated that there are miRNAs changes during EV71 pathogenesis and EV71 utilise host miRNAs to attenuate antiviral pathways during infection. Together, data from this study provide critical information on the role of miRNAs during EV71 infection.
Highlights
Hand, Foot and Mouth Disease (HFMD) is a contagious viral disease that commonly affects infants and children, with blisters and flu like symptoms [1,2,3,4,5,6]
We explore the role of miRNAs in the pathogenesis of EV71 infected HT29 cells and identified key miRNA changes due to EV71 infection which might play a key role during EV71 pathogenesis
DGCR8, an essential cofactor for microRNAs biogenesis contribute to a central role during EV71 pathogenesis
Summary
Foot and Mouth Disease (HFMD) is a contagious viral disease that commonly affects infants and children, with blisters and flu like symptoms [1,2,3,4,5,6]. Unlike other HFMD causing enteroviruses, EV71 is commonly associated with severe clinical diseases, including neurological diseases such as aseptic meningitis, brainstem and cerebellar encephalitis leading to cardiopulmonary failure and death [3,10,11,12,13]. Viruses attenuate host gene expression to enhance their survival [14,15,16,17,18]. Such activities include altering the cellular microenvironment to allow successful virus replication and evasion of the host immune system [19]
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