Impact of Borna Disease Virus Infection on the Transcriptome of Differentiated Neuronal Cells and Its Modulation by Antiviral Treatment

Viruses. 2023 Apr 10;15(4):942. doi: 10.3390/v15040942.

Abstract

Borna disease virus (BoDV-1) is a highly neurotropic RNA virus that causes neurobehavioral disturbances such as abnormal social activities and memory impairment. Although impairments in the neural circuits caused by BoDV-1 infection induce these disturbances, the molecular basis remains unclear. Furthermore, it is unknown whether anti-BoDV-1 treatments can attenuate BoDV-1-mediated transcriptomic changes in neuronal cells. In this study, we investigated the effects of BoDV-1 infection on neuronal differentiation and the transcriptome of differentiated neuronal cells using persistently BoDV-1-infected cells. Although BoDV-1 infection did not have a detectable effect on intracellular neuronal differentiation processes, differentiated neuronal cells exhibited transcriptomic changes in differentiation-related genes. Some of these transcriptomic changes, such as the decrease in the expression of apoptosis-related genes, were recovered by anti-BoDV-1 treatment, while alterations in the expression of other genes remained after treatment. We further demonstrated that a decrease in cell viability induced by differentiation processes in BoDV-1-infected cells can be relieved with anti-BoDV-1 treatment. This study provides fundamental information regarding transcriptomic changes after BoDV-1 infection and the treatment in neuronal cells.

Keywords: Borna disease virus; antiviral; differentiation; gene expression; neuronal cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antiviral Agents
  • Borna Disease* / genetics
  • Borna Disease* / metabolism
  • Borna disease virus* / genetics
  • Cell Differentiation
  • Transcriptome

Substances

  • Antiviral Agents

Grants and funding

This study was supported in part by JSPS KAKENHI (Grant Numbers JP18H02664, JP18K19449, JP21H02738 and JP22K19436) and grants from the Takeda Science Foundation, Kobayashi International Scholarship Foundation, The Naito Foundation, SEI Group CSR Foundation, Ryobi Teien Memory Foundation, and Suzuken Memorial Foundation.