Skip to main page content
U.S. flag

An official website of the United States government

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2020 Aug 28:11:578599.
doi: 10.3389/fphar.2020.578599. eCollection 2020.

Mitochondria Targeted Viral Replication and Survival Strategies-Prospective on SARS-CoV-2

Priya Gatti  1   2 , Hema Saranya Ilamathi  1   2 , Kiran Todkar  1   2 , Marc Germain  1   2
Affiliations
Review

Mitochondria Targeted Viral Replication and Survival Strategies-Prospective on SARS-CoV-2

Priya Gatti et al. Front Pharmacol. .

Abstract

SARS-CoV-2 is a positive sense RNA coronavirus that constitutes a new threat for the global community and economy. While vaccines against SARS-CoV-2 are being developed, the mechanisms through which this virus takes control of an infected cell to replicate remains poorly understood. Upon infection, viruses completely rely on host cell molecular machinery to survive and replicate. To escape from the immune response and proliferate, viruses strategically modulate cellular metabolism and alter subcellular organelle architecture and functions. One way they do this is by modulating the structure and function of mitochondria, a critical cellular metabolic hub but also a key platform for the regulation of cellular immunity. This versatile nature of mitochondria defends host cells from viruses through several mechanisms including cellular apoptosis, ROS signaling, MAVS activation and mitochondrial DNA-dependent immune activation. These events are regulated by mitochondrial dynamics, a process by which mitochondria alter their structure (including their length and connectivity) in response to stress or other cues. It is therefore not surprising that viruses, including coronaviruses hijack these processes for their survival. In this review, we highlight how positive sense RNA viruses modulate mitochondrial dynamics and metabolism to evade mitochondrial mediated immune response in order to proliferate.

Keywords: RNA viruses; SARS-CoV-2; immune response; metabolism; mitochondria; mitochondrial dynamics.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Effects of (+)ssRNA viruses on mitochondrial dynamics and function. By manipulating mitochondrial dynamics (1), (+)ssRNA viruses either directly or indirectly manipulate a number of cellular processes to promote viral replication and immune evasion. These include increasing mitochondrial activity (2), inhibiting MAVS activation (3) and activating mitophagy (4) to prevent apoptosis (5). In the case of SARS-CoV (and probably SARS-CoV-2), the ORF9b protein can perform most of these functions.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Abrisch R. G., Gumbin S. C., Wisniewski B. T., Lackner L. L., Voeltz G. K. (2020). Fission and fusion machineries converge at ER contact sites to regulate mitochondrial morphology. J. Cell Biol. 219 (4), e201911122. 10.1083/jcb.201911122 - DOI - PMC - PubMed
    1. Antico Arciuch V. G., Elguero M. E., Poderoso J. J., Carreras M. C. (2012). Mitochondrial Regulation of Cell Cycle and Proliferation. Antioxid. Redox Signaling 16 (10), 1150–1180. 10.1089/ars.2011.4085 - DOI - PMC - PubMed
    1. Barbier V., Lang D., Valois S., Rothman A. L., Medin C. L. (2017). Dengue virus induces mitochondrial elongation through impairment of Drp1-triggered mitochondrial fission. Virology 500, 149–160. 10.1016/j.virol.2016.10.022 - DOI - PMC - PubMed
    1. Bohovych I., Khalimonchuk O. (2016). Sending Out an SOS: Mitochondria as a Signaling Hub. Front. Cell Dev. Biol. 4, 109. 10.3389/fcell.2016.00109 - DOI - PMC - PubMed
    1. Bordi L., Castilletti C., Falasca L., Ciccosanti F., Calcaterra S., Rozera G., et al. (2005). Bcl-2 inhibits the caspase-dependent apoptosis induced by SARS-CoV without affecting virus replication kinetics. Arch. Virol. 151 (2), 369–377. 10.1007/s00705-005-0632-8 - DOI - PMC - PubMed