Abstract
MicroRNAs respond to the inflammatory responses induced by RNA virus infection. In this study, we investigated the specific microRNA profile in the peripheral blood of infants infected with respiratory syncytial virus (RSV). Blood specimens were analyzed using microRNA microarrays, followed by quantitative RT-PCR. A specific microRNA profile in the peripheral blood of RSV-infected infants was identified for the first time. MiR-106b-5p, miR-20b-5p, and miR-342-3p were upregulated, while miR-320e, miR-320d, miR-877-5p, miR-122-5p, and miR-92b-5p were downregulated. Pathway analysis indicated that the dysregulated microRNAs were involved in inflammatory and immune responses, including Wnt, TGF-β, insulin, and T and B cell receptor signaling. These results demonstrate that RSV infection associates with a distinct microRNA fingerprint and suggest that RSV induces inflammatory responses in infants.
Highlights
Respiratory syncytial virus (RSV) is an enveloped negative strand RNA virus, which belongs to the Paramyxoviridae family
Differential expression analysis of miRNA microarrays between RSV patients and healthy controls indicated that 37 miRNAs were upregulated-fold-change ≥ 2, while 24 miRNAs were downregulated, and 72 miRNAs were not changed
There was no significant change of miR-320e in all five RSV infected cases, and let-7c5p was downregulated in RSV1, RSV2, and RSV3, while there was no difference in RSV4 and RSV5
Summary
Respiratory syncytial virus (RSV) is an enveloped negative strand RNA virus, which belongs to the Paramyxoviridae family. Infants with RSV infection often develop severe bronchiolitis or pneumonia [1]. The lack of understanding of the host-virus interface has hindered prevention and treatment methods, as well as a successful RSV vaccine development [2]. Even though recent antiviral efforts have begun to inhibit virus replication by targeting host pathways and using interfering RNAs [36], regulation of the host immune responses resulting in bronchiolitis remains a challenge. Viral infections can influence host miRNA production. Host miRNAs can regulate the viral life cycle, and target the viral messenger RNA [12]
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