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Use of Viral Entry Assays and Molecular Docking Analysis for the Identification of Antiviral Candidates against Coxsackievirus A16
Published on: July 15, 2019
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Transcriptome analysis reveals dynamic changes in coxsackievirus A16 infected HEK 293T cells
Jun Jin1, Rujiao Li2, Chunlai Jiang1,3
1National Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun, 130012, China.
BMC Genomics
|February 16, 2017
Summary
Coxsackievirus A16 (CVA16) infection up-regulates SCARB2, potentially increasing co-infections. This study reveals transcriptome changes and key miRNAs involved in hand, foot, and mouth disease (HFMD) pathogenesis.
Area of Science:
- Virology
- Molecular Biology
- Genomics
Background:
- Coxsackievirus A16 (CVA16) and enterovirus 71 (EV71) are primary causes of hand, foot, and mouth disease (HFMD).
- The host cell transcriptome response to CVA16 infection remains largely uncharacterized.
Purpose of the Study:
- To investigate the mRNA and miRNA expression profiles of human embryonic kidney 293T cells following CVA16 infection.
- To identify host factors and pathways involved in CVA16 pathogenesis and HFMD.
Main Methods:
- Comparative analysis of mRNA and miRNA expression profiles in CVA16-infected versus non-infected 293T cells.
- Correlation analysis to link miRNA expression with target genes.
Main Results:
- SCARB2 transcription was significantly upregulated (nearly 10-fold) in CVA16-infected cells, potentially facilitating co-infection with EV71.
- Down-regulation of has-miR-3605-5p was associated with increased SCARB2 expression.
- Differentially expressed genes were enriched in extracellular membrane (ECM)-receptor interaction and circadian rhythm pathways, potentially linked to HFMD clinical symptoms.
- hsa-miR-149-3p and hsa-miR-5001-5p were implicated in up-regulating morbigenous pathways.
Conclusions:
- CVA16 infection alters the host cell transcriptome, notably upregulating SCARB2 and genes in ECM-receptor interaction and circadian rhythm pathways.
- Key miRNAs, including has-miR-3605-5p, hsa-miR-149-3p, and hsa-miR-5001-5p, play regulatory roles in CVA16-induced pathogenesis.
- These findings offer new insights into the molecular mechanisms underlying HFMD caused by CVA16.

