Nikhil Prasad Fact checked by:Thailand Medical News Team Oct 31, 2024 1 month, 1 week, 4 days, 17 hours, 43 minutes ago
Medical News: Viruses have long been known to manipulate host cells for survival, but new findings reveal they target one of the most critical components of our cells: the mitochondria. Recent studies led by researchers from the Centro de Investigación Veterinaria de Tandil in Argentina and the Medical University of South Carolina show that viruses can disrupt mitochondrial function and metabolism, which has far-reaching implications for health. This
Medical News report explores how viral infections cause mitochondrial dysfunction and metabolic chaos in cells.
Mitochondrial Dysfunction and Metabolic Chaos in Viral Infections
The Role of Mitochondria in Viral Infections
Mitochondria are not only powerhouses generating energy for cells, but they also play a vital role in our immune defenses. Viruses, as intracellular parasites, exploit mitochondria to sustain their own life cycle. They modify mitochondria to ensure they get energy and macromolecules needed for survival. But the viral takeover doesn’t stop there. Viruses also target mitochondrial functions related to immune responses, altering the balance of cellular metabolism and even causing oxidative stress.
Oxidative Stress: Fueling Viral Replication
Viruses can disrupt mitochondrial function and cause an increase in reactive oxygen species (ROS), which can harm the cell. These ROS particles can attack cell structures, leading to inflammation and cellular damage. Some viruses thrive in oxidative environments, enhancing their replication. For example, Dengue virus (DENV) and Japanese Encephalitis Virus (JEV) induce oxidative stress in neurons, contributing to neurological damage. In this viral takeover, ROS supports viral spread by encouraging inflammation, an immune response that can inadvertently aid the virus.
In some cases, viruses like HIV manipulate ROS levels to prevent infected cells from undergoing programmed cell death, ensuring they remain in the body long-term. Through an increased ROS balance, viruses manage to outlive immune defenses, increasing the chance of chronic infections and further damage to host tissues.
Viral Metabolism: The Warburg Effect
During infection, viruses require significant energy and resources. To meet these needs, viruses can rewire cellular metabolism. Many viruses, such as Epstein-Barr virus (EBV) and Human Cytomegalovirus (HCMV), trigger a metabolic shift known as the "Warburg Effect" in which cells rely more on glycolysis (sugar breakdown) than normal respiration, even in the presence of oxygen. This shift provides the virus with a quick supply of energy and building blocks for replication.
Some viruses stimulate a reverse Warburg effect, where neighboring cells produce and supply the virus with necessary metabolites, fueling infections like Kaposi’s Sarcoma-Associated Herpesvirus (KSHV). The viral proteins can alter mitochondrial function, promoting a metabolic switch and keeping the cells in a "growth" mode that enhances viral survival.
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Lipid Alterations: Fueling Viral Factories
Lipids are critical for virus assembly, replication, and persistence. Lipid droplets, small organelles storing fats, are often recruited by viruses as resources. Some viruses like Hepatitis B virus (HBV) cause lipid build-ups in cells. This allows viruses to use lipids as fuel for replication, contributing to diseases such as liver steatosis, a condition marked by excess fat in the liver. Viruses also use oxidative processes to degrade cellular membranes, which supports their ability to move within cells. SARS-CoV-2, the virus behind COVID-19, was found to alter fatty acid metabolism for its replication needs.
Immune System Evasion Tactics
Mitochondria are essential for immune responses, especially for signaling proteins like MAVS that activate antiviral responses. However, viruses like SARS-CoV-2 have developed ways to suppress MAVS, weakening the cell's antiviral defenses. By targeting these immune proteins, viruses evade early detection by the immune system, thus avoiding destruction.
Human cytomegalovirus (HCMV), for instance, blocks key mitochondrial functions, enabling it to evade immune responses. These strategies highlight how viruses carefully manipulate mitochondria to stay undetected, allowing them to persist in the host and sometimes even progress to a chronic infection.
Conclusion
The study findings underscore that mitochondria play a more extensive role in viral infections than previously understood. Viruses hijack mitochondrial functions to survive, disabling immune responses, altering metabolism, and inducing oxidative stress. Understanding these complex interactions opens avenues for new antiviral treatments that could disrupt viral use of mitochondria without harming normal cellular functions.
The study findings were published in the peer-reviewed journal: Cells.
https://www.mdpi.com/2073-4409/13/21/1789
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Read Also:
https://www.thailandmedical.news/news/new-insights-into-mitochondrial-role-in-post-covid-recovery-and-long-covid-progression
https://www.thailandmedical.news/news/the-f17-protein-of-all-poxviruses-including-mpox-counteracts-mitochondrially-orchestrated-antiviral-responses
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