Endoplasmic reticulum & mitochondrial calcium homeostasis: The interplay with viruses

Calcium ions (Ca2+) act as secondary messengers in a plethora of cellular processes and play crucial role in cellular organelle function and homeostasis. The average resting concentration of Ca2+ is nearly 100 nM and in certain cells it can reach up to 1 mu M. The high range of Ca2+ concentration across the plasma membrane and intracellular Ca2+ stores demands a well-coordinated maintenance of free Ca2+ via influx, efflux, buffering and storage. Endoplasmic Reticulum (ER) and Mitochondria depend on Ca2+ for their function and also serve as major players in intracellular Ca2+ homeostasis. The ER-mitochondria interplay helps in orchestrating cellular calcium homeostasis to avoid any detrimental effect resulting from Ca2+ overload or depletion. Since Ca2+ plays a central role in many biological processes it is an essential component of the virus-host interactions. The large gradient across membranes enable the viruses to easily modulate this buffered environment to meet their needs. Viruses exploit Ca2+ signaling to establish productive infection and evade the host immune defense. In this review we will detail the interplay between the viruses and cellular & ER-mitochondrial calcium signaling and the significance of these events on viral life cycle and disease pathogenesis.

Automated summary

Calcium ions serve as secondary messengers in cellular processes, with ER and mitochondria relying on Ca2+ for their function. Viruses exploit Ca2+ signaling to establish infection and evade host immune defenses, highlighting the significance of this interplay on viral life cycles and disease pathogenesis.