Viral Infection Modulates Mitochondrial Function.

Xiaowen Li,Keke Wu,Sen Zeng,Feifan Zhao,Zhaoyao Li,Shuangqi Fan,Jinding Chen,Hongxing Ding,Jindai Fan,Mingqiu Zhao,Lin Yi

doi:10.3390/ijms22084260

Abstract

Mitochondria are important organelles involved in metabolism and programmed cell death in eukaryotic cells. In addition, mitochondria are also closely related to the innate immunity of host cells against viruses. The abnormality of mitochondrial morphology and function might lead to a variety of diseases. A large number of studies have found that a variety of viral infections could change mitochondrial dynamics, mediate mitochondria-induced cell death, and alter the mitochondrial metabolic status and cellular innate immune response to maintain intracellular survival. Meanwhile, mitochondria can also play an antiviral role during viral infection, thereby protecting the host. Therefore, mitochondria play an important role in the interaction between the host and the virus. Herein, we summarize how viral infections affect microbial pathogenesis by altering mitochondrial morphology and function and how viruses escape the host immune response.

Highlights

Mitochondria are important organelles involved in metabolism and programmed cell death in eukaryotic cells
Mfns contain heptad repeat regions (HR2), and Mfn1 and Mfn2, located on the outer mitochondrial membrane (OMM), interact to form Mfn1/Mfn2 homodimers or Mfn1/Mfn2 heterodimers through oligomerization of the HR2 structures, thereby promoting phase trans-plugging of the adjacent OMM [6,7], and involving GTP hydrolysis, which eventually leads to the fusion of the OMM [8,9]
OPA1 protein was hydrolyzed into different fragments in the intermembrane space: one is the long subtype L-OPA1 associated with mitochondrial fusion, the other is the short subtype S-OPA1 [10,11]

Summary

Physiological Morphology of Mitochondria

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Mitochondria maintain the dynamic balance of the mitochondrial network through the fission and fusion mediated by a dedicated set of dynamin-related GTPases, provide energy for cells, and regulate processes such as autophagy, calcium homeostasis, innate immunity, signal transduction, and apoptosis [1]. Loss of fusion-mediating proteins (MFN1, MFN2, and OPA1) can cause changes in mitochondrial morphology, leading to mitochondrial fragmentation. Drp is a significant protein that mediates mitochondrial fission. RIP1 phosphorylates Ser616 residue of Drp, thereby inducing mitochondrial fission and eliminating damaged mitochondria through mitophagy, when cells are in a state of energy stress [15]. Mitochondrial dynamics proteins (MiDs) are involved in mitochondrial fission in fis and Drp deficient cells. We explore how viruses manipulate mitochondria and how this manipulation affects microbial pathogenesis

Viral Infection Disrupts Mitochondrial Dynamics

Viral Infection Regulates Mitochondria-Induced Cell Death

Viral Infection Regulates Mitochondria-Induced Innate Immunity

Viral Infection Regulates Mitochondrial Metabolism

Findings

Concluding Remarks