Key result
Coxsackievirus A10 infection significantly alters over 300 miRNAs in bronchial epithelial cells.
Why the study?
The role of host cellular microRNAs in defending against Coxsackievirus A10 infection and the disease pathogenesis remains unclear.
p-value: p=<0.05
This study identifies differentially expressed miRNAs in bronchial epithelial cells following CV-A10 infection, providing insights into host immune responses and viral pathogenesis.
Altered miRNA profiles in infected cells warrant caution extrapolating to patients; hypothesis-generating and requires in vivo validation before clinical relevance.
Coxsackievirus A10 (CV-A10), the causative agent of hand, foot, and mouth disease (HFMD), caused a series of outbreaks in recent years and often leads to neurological impairment, but a clear understanding of the disease pathogenesis and host response remains elusive. Cellular microRNAs (miRNAs), a large family of non-coding RNA molecules, have been reported to be key regulators in viral pathogenesis and virus-host interactions. However, the role of host cellular miRNAs defensing against CV-A10 infection is still obscure. To address this issue, we systematically analyzed miRNA expression profiles in CV-A10-infected 16HBE cells by high-throughput sequencing methods in this study. It allowed us to successfully identify 312 and 278 miRNAs with differential expression at 12 h and 24 h post-CV-A10 infection, respectively. Among these, 4 miRNAs and their target genes were analyzed by RT-qPCR, which confirmed the sequencing data. Gene target prediction and enrichment analysis revealed that the predicted targets of these miRNAs were significantly enriched in numerous cellular processes, especially in regulation of basic physical process, host immune response and neurological impairment. And the integrated network was built to further indicate the regulatory roles of miRNAs in host-CV-A10 interactions. Consequently, our findings could provide a beneficial basis for further studies on the regulatory roles of miRNAs relevant to the host immune responses and neuropathogenesis caused by CV-A10 infection.
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Hu et al. (2022) studied Coxsackievirus A10 (CV-A10) infection. Coxsackievirus A10 (CV-A10) infection vs. Uninfected cells (0 hpi) was evaluated on Differentially expressed miRNAs (p=<0.05). Coxsackievirus A10 infection of 16HBE bronchial epithelial cells significantly altered the expression of 312 and 278 miRNAs at 12 and 24 hours post-infection, respectively.
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