Different inhibitory effects on the proliferation and apoptosis of human and laboratory Borna disease virus‑infected human neuroblastoma SH‑SY5Y cells in vitro.

Borna disease virus (BDV) is a neurotropic and non‑cytolytic virus, which causes behavioral disorders in a wide range of warm‑blooded species. It is well established that BDV induces neurodegeneration by impairing neurogenesis and interfering with neuronal functioning in the limbic system. In the present study, the potential role of BDV infection in SH‑SY5Y cells was identified, and comparisons of two original BDV strains (the human Hu‑H1 and the laboratory Strain V) were performed to further elucidate the phenotypes of BDV pathogenesis with strain differences. Cell Counting Kit‑8 and flow cytometric analyses revealed that the two BDV strain‑infected groups exhibited marked anti‑proliferation and cell cycle arrest compared with the control group, and the Hu‑H1 strain caused more evident effects. However, the Hu‑H1 strain did not exert effects on the apoptosis of SH‑SH5Y cells, while Strain V led to a marked increase in apoptosis upon initial infection. Western blot analysis confirmed the upregulation of apoptosis regulator BAX protein and the downregulation of apoptosis regulator Bcl‑2 protein caused by the two BDV strains. The results of the present study provided evidence that infection with BDV suppressed SH‑SY5Y cellular functioning and exhibited divergent antiproliferative and apoptotic roles in cells between the two strains. The present study provided an insight for future investigation of strain differences and underlying pathomechanisms.