PMC:7247521 / 45480-46732 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7247521","sourcedb":"PMC","sourceid":"7247521","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7247521","text":"It has been reported that host cellular microRNAs (miRNAs) are involved in the regulation of virus infection [41]. A previous study discovered that significantly up-regulated MIR301 and down-regulated MIR183/130B were found in H1N1 patients [42]. Consistent with these results, we found that MIR183 and MIR130A/B/301 are related to four functional units of QFPD, indicating these microRNAs may exert anti−COVID-19 activity through QFPD. In addition, CDKs have played a role in the efficient replication of various viruses, including human HIV-1, papillomaviruses, human cytomegalovirus (HCMV), herpes simplex virus (HSV) type 1 and HSV-2 [43,44]. In agreement with these results, we found that CDK7 was predicted to enriched in the five formulae, suggesting that QFPD may regulate replication of COVID-19 viruses via CDK7 mediated cell cycle and RNA polymerase II transcription. Recently, a previous study showed that LXR known to regulate cholesterol homeostasis during inflammation were differentially regulated during H1N1 influenza virus infection [45]. Based on our results that LXR was associated with MSXG, SGMH, XCH, WLS targets, we speculated that QFPD can regulate metabolic and pro-inflammatory processes to counter COVID-19 virus 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