Abstract
Long-term studies have shown that virus infection affects the energy metabolism of host cells, which mainly affects the function of mitochondria and leads to the hydrolysis of ATP in host cells, but it is not clear how virus infection participates in mitochondrial energy metabolism in host cells. In our study, HUVEC cells were infected with HSV-1, and the differentially expressed genes were obtained by microarray analysis and data analysis. The viral gene encoding protein UL16 was identified to interact with host protein ANT2 by immunoprecipitation and mass spectrometry. We also reported that UL16 transfection promoted oxidative phosphorylation of glucose and significantly increased intracellular ATP content. Furthermore, UL16 was transfected into the HUVEC cell model with mitochondrial dysfunction induced by d-Gal, and it was found that UL16 could restore the mitochondrial function of cells. It was first discovered that viral protein UL16 could enhance mitochondrial function in mammalian cells by promoting mitochondrial metabolism. This study provides a theoretical basis for the prevention and treatment of mitochondrial dysfunction or the pathological process related to mitochondrial dysfunction.
Highlights
Long-term studies have shown that virus infection affects the energy metabolism of host cells, which mainly affects the function of mitochondria and leads to the hydrolysis of ATP in host cells, but it is not clear how virus infection participates in mitochondrial energy metabolism in host cells
The previously identified differentially expressed proteins are closely related to mitochondria, we try to find out the relationship between mitochondrial specific viral protein and energy metabolism. we examined the mitochondrial functions in UL16 transfected cells
Our study shows that Herpes simplex virus 1 (HSV-1) UL16 protein can target Adenine nucleotide transporter 2 (ANT2) protein on the mitochondrial membrane of host cells, activate the cellular energy metabolism pathway, and significantly increase the content of intracellular ATP
Summary
Long-term studies have shown that virus infection affects the energy metabolism of host cells, which mainly affects the function of mitochondria and leads to the hydrolysis of ATP in host cells, but it is not clear how virus infection participates in mitochondrial energy metabolism in host cells. HSV-1 relies on the metabolic network of the host cells to provide energy and macromolecular precursors to fuel viral replication. Some viral infections enhance mitochondrial metabolism and activate the tricarboxylic acid cycle to provide energy and intermediate metabolites as power and raw materials for virus replication and a ssembly[12]. The excessive expression of viral protein in the hepatitis C. virus (HCV) can cause a change of mitochondrial membrane potential, inhibit oxidative phosphorylation and increase the production of ATP, which may be the reason for the conversion of energy to g lycolysis[15]. It is of great significance to reveal the pathogenic mechanism of the virus to the host by studying the morphology and function of cell mitochondria after virus infection. UL12.5 protein targets mitochondria and degrades mitochondrial DNA by nuclease function early in viral infection[19]
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