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Human Cytomegalovirus Alters Host Cell Mitochondrial Function during Acute Infection
Joseph A Combs1, Elizabeth B Norton1, Zubaida R Saifudeen2
1Department of Microbiology and Immunology, Tulane University School of Medicine, New Orleans, Louisiana, USA.
Journal of Virology
|November 8, 2019
Summary
Human cytomegalovirus (HCMV) infection increases host cell mitochondrial activity, including oxidative phosphorylation. HCMV replication critically depends on the host cell
Area of Science:
- Cell Biology
- Virology
- Metabolic Research
Background:
- Human cytomegalovirus (HCMV) is a prevalent herpesvirus causing significant pathologies, especially in immunocompromised individuals and as a leading cause of infectious birth defects.
- Existing knowledge indicates HCMV infection increases host cell glycolysis, but its impact on oxidative phosphorylation and mitochondria remained less defined.
- Current therapeutic strategies against HCMV, including vaccines and antivirals, face limitations due to ineffectiveness, side effects, and resistance development.
Purpose of the Study:
- To investigate the effects of HCMV infection on host cell mitochondrial morphology, function, and bioenergetics.
- To determine the role of host cell mitochondria, specifically the electron transport chain (ETC), in HCMV replication.
- To explore host cell mitochondria as a potential therapeutic target for HCMV infection.
Main Methods:
- Analysis of mitochondrial morphology, including network dynamics (fission and fusion events), mass, and membrane potential in HCMV-infected cells.
- Assessment of electron transport chain (ETC) activity and reactive oxygen species (ROS) production.
- Evaluation of HCMV replication in cells with depleted mitochondrial DNA (mtDNA).
Main Results:
- HCMV infection induces mitochondrial fission, increased mitochondrial mass, and elevated membrane potential.
- The ETC functions at a higher rate, leading to increased ROS production, yet the mitochondria meet the host cell's demands.
- Depletion of mtDNA severely impairs HCMV replication, highlighting the essential role of the host cell ETC.
Conclusions:
- Host cell mitochondria undergo significant functional and morphological changes during HCMV infection to support viral replication.
- The host cell's electron transport chain is essential for HCMV replication, suggesting a critical dependency.
- Targeting host cell mitochondria presents a promising strategy for developing novel antiviral therapies against HCMV.
