4.5 Article

Global expression and functional analysis of human piRNAs during HSV-1 infection

Journal

VIRUS RESEARCH
Volume 328, Issue -, Pages -

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ELSEVIER
DOI: 10.1016/j.virusres.2023.199087

Keywords

HSV-1; piRNA; RNA-seq; Expression pattern; Viral replication

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This study systematically investigated the expression characteristics of piRNAs in HSV-1-infected human lung fibroblasts and identified 69 differentially expressed piRNAs. These piRNAs were mainly involved in antiviral immunity and various human disease-related signaling pathways. Furthermore, two piRNAs that potentially regulate HSV-1 replication were screened.
Piwi-interacting RNAs (piRNAs) are a class of non-coding RNAs that play a key role in spermatogenesis. How-ever, little is known about their expression characterization and role in somatic cells infected with herpes simplex virus type 1 (HSV-1). In this study, we systematically investigated the cellular piRNA expression profiles of HSV-1-infected human lung fibroblasts. Compared with the control group, 69 differentially expressed piRNAs were identified in the infection group, among which 52 were up-regulated and 17 were down-regulated. The changes in the expression of 8 piRNAs were further verified by RT-qPCR with a similar expression trend. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis showed that the target genes of piRNAs were mainly involved in antiviral immunity and various human disease-related signaling pathways. Furthermore, we tested the effects of four up-regulated piRNAs on viral replication by transfecting piRNA mimics. The results showed that the virus titers of the group transfected with piRNA-hsa-28,382 (alias piR-36,233) mimic decreased significantly, and that of the group transfected piRNA-hsa-28,190 (alias piR-36,041) mimic significantly increased. Overall, our results revealed the expression characteristics of piRNAs in HSV-1-infected cells. We also screened two piRNAs that potentially regulate HSV-1 replication. These results may promote a better understanding of the regulatory mechanism of pathophysiological changes induced by HSV-1 infection.

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