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Background <p>Japanese encephalitis virus (JEV) is an arbovirus which is the most common virus in the genus <i>Orthoflavivirus</i> that causes significant viral encephalitis with a high fatality rate and is distributed throughout Asian countries. JEV infection induces brain tissue disease characterized by neuronal death. We previously demonstrated that JEV elevates the formation of an N-terminal truncated version of BAX (p18 BAX), triggering mitochondria-mediated apoptosis. However, the mechanisms by which virus-host interactions induce the generation of p18 BAX during JEV infection are unclear.</p> Methods <p>The present study aims to investigate the underlying mechanism by which JEV-induced cell apoptosis is mediated by the activation of calpain-induced proteolytic cleavage of BAX. Calpeptin, a calpain inhibitor, was used to evaluate the effect on calpain activity, cell viability, and apoptotic molecules expression in JEV-infected neuroblastoma SH-SY5Y cells.</p> Results <p>Our data showed that JEV infection resulted in the activation of the calpain-mediated apoptosis pathway, as evidenced by increased calpain activation and p18 BAX generation. The translocation of p18 BAX to the mitochondria results in cytochrome c release and increased of caspase-3 activity, resulting in an increase of cleaved PARP expression, which induced neuronal apoptosis. Inhibiting calpain activity by calpeptin attenuated all these effects.</p> Conclusions <p>Our results reveal that JEV induces neuronal cell apoptosis by activating calpain-mediated cleavage of BAX. These findings provide a novel insight into JEV-caused encephalitis and suggest that calpain inhibition may represent a potential therapeutic strategy.</p>

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Inhibition of calpain-mediated BAX cleavage attenuates Japanese encephalitis virus-induced apoptosis in SH-SY5Y neuroblastoma cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月2日

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  • Kuntida Kitidee,
  • Arisara Samutpong,
  • Nattaporn Pakpian,
  • Montri Yasawong,
  • Prapimpun Wongchitrat

摘要

Background

Japanese encephalitis virus (JEV) is an arbovirus which is the most common virus in the genus Orthoflavivirus that causes significant viral encephalitis with a high fatality rate and is distributed throughout Asian countries. JEV infection induces brain tissue disease characterized by neuronal death. We previously demonstrated that JEV elevates the formation of an N-terminal truncated version of BAX (p18 BAX), triggering mitochondria-mediated apoptosis. However, the mechanisms by which virus-host interactions induce the generation of p18 BAX during JEV infection are unclear.

Methods

The present study aims to investigate the underlying mechanism by which JEV-induced cell apoptosis is mediated by the activation of calpain-induced proteolytic cleavage of BAX. Calpeptin, a calpain inhibitor, was used to evaluate the effect on calpain activity, cell viability, and apoptotic molecules expression in JEV-infected neuroblastoma SH-SY5Y cells.

Results

Our data showed that JEV infection resulted in the activation of the calpain-mediated apoptosis pathway, as evidenced by increased calpain activation and p18 BAX generation. The translocation of p18 BAX to the mitochondria results in cytochrome c release and increased of caspase-3 activity, resulting in an increase of cleaved PARP expression, which induced neuronal apoptosis. Inhibiting calpain activity by calpeptin attenuated all these effects.

Conclusions

Our results reveal that JEV induces neuronal cell apoptosis by activating calpain-mediated cleavage of BAX. These findings provide a novel insight into JEV-caused encephalitis and suggest that calpain inhibition may represent a potential therapeutic strategy.