Calcium (Ca²⁺) plays fundamental and diverse roles in brain cells as a second messenger of many signaling pathways. Given the high energy demand in the brain and the generally non-regenerative state of neurons, the role of brain mitochondrial calcium [Ca²⁺]_m in particular, in regulating ATP generation and determination of cell fate by initiation or inhibition of programmed cell death (PCD) becomes critical. Since [Ca²⁺]_m signaling has a central role in brain physiology, it represents an ideal target for viruses to hijack the Ca²⁺ machinery to favor their own persistence, replication and/or dissemination by modulating cell death. This review discusses the ways by which neurotropic viruses are known to exploit the [Ca²⁺]_m signaling of their host cells to regulate cell death in the brain, particularly in neurons. We hope our review will highlight the importance of [Ca²⁺]_m handling in the virus-infected brain and stimulate further studies towards exploring novel [Ca²⁺]_m related therapeutic strategies for viral effects on the brain.

钙 (Ca ²⁺ ) 作为许多信号通路的第二信使，在脑细胞中发挥着基本而多样的作用。鉴于大脑中的高能量需求和神经元的一般非再生状态，特别是大脑线粒体钙 [Ca ²⁺ ] _m在调节 ATP 生成和通过启动或抑制程序性细胞死亡来确定细胞命运中的作用(PCD) 变得至关重要。由于 [Ca ²⁺ ] _m信号在脑生理学中具有核心作用，因此它代表了病毒劫持 Ca ^{2+的理想目标}通过调节细胞死亡来支持它们自身的持久性、复制和/或传播的机制。这篇综述讨论了已知嗜神经病毒如何利用宿主细胞的 [Ca ²⁺ ] _m信号来调节大脑中的细胞死亡，特别是在神经元中。我们希望我们的审查将突出 [Ca ²⁺ ] _m在病毒感染的大脑中处理的重要性，并促进进一步研究探索新的 [Ca ²⁺ ] _m相关治疗策略，以解决病毒对大脑的影响。