Viral Infection Modulates Mitochondrial Function

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.

Keywords: apoptosis; host innate immunity; mitochondrial fission and fusion; virus infection.

Figure 1

Viral infection disrupts mitochondrial dynamics. Different viruses affect mitochondrial dynamics through mitochondrial fusion proteins (MFNs, OPA1) or fission proteins (DRP1) and induce mitophagy to clear damaged mitochondria to enhance cell survival and viral persistence.

Figure 2

Viral infection regulates mitochondria-induced cell death. Different viruses mediate B-cell lymphoma 2 (Bcl-2) family proteins, release Cyt c, activate procaspase-9, and form apoptosomes, thereby inducing cell apoptosis.

Figure 3

Viral infection regulates mitochondria-induced innate immunity. After the virus invades the cell, RLRs recognize the viral RNA and interact with the mitochondrial antiviral signal (MAVS) to activate the antiviral signal pathway. Different viruses evade host innate immunity by blocking the RLR signaling pathway.