Journal
MITOCHONDRION
Volume 58, Issue -, Pages 227-242Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.mito.2021.03.008
Keywords
Virus; Calcium; Mitochondria; Mitochondrial calcium uniporter; Calcium homeostasis; Antiviral signaling
Categories
Funding
- DBTWellcome Trust India Alliance [IA/I/15/1/501826]
- DST SERB [CRG/2020/006238/BHS]
- Institute of Life Sciences (ILS), Bhubaneswar
- National Postdoctoral Fellowship [PDF/2019/001189]
Ask authors/readers for more resources
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.
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available