What you need to know
SARS-CoV-2, the virus that causes COVID-19, can damage the lungs, heart, brain, kidneys, and blood vessels. Inflammation was first thought to be the main source of this damage. As it became clear that parts of the virus bind to proteins in the mitochondria — the parts of the cell that produce most cellular energy — researchers realized that compromised mitochondria may also play a role in organ damage from SARS-CoV-2 infection.
In a study supported by the National Institute of Allergy and Infectious Diseases (NIAID), researchers found that SARS-CoV-2 can cause lasting damage to the energy production of mitochondria in many organs of the body.
What did the researchers do?
Researchers compared mitochondrial gene expression (when genes are activated) in tissue samples from the throats of 216 people with COVID-19 and 519 uninfected people. The researchers also compared mitochondrial function in autopsy samples from the hearts, kidneys, livers, lungs, and lymph nodes of 35 people who died from COVID-19 and 5 people who died from other causes.
The researchers found that during acute SARS-CoV-2 infection, mitochondrial genes were suppressed in the nasopharynx (the uppermost part of the nose and throat). Once the virus was cleared from the body, those genes stayed suppressed in tissue samples from the heart, kidney, liver, and lymph nodes, indicating potential long-term damage in those organs. However, the genes in the lungs did not stay suppressed after the infection cleared.
When the researchers used animal models to track mitochondrial function over the entire course of infection, they saw similar results: Energy production that was suppressed in the lungs during early infection bounced back once the immune system brought the virus under control. At the same time, mitochondrial gene expression was altered in the brain during early infection, even though no SARS-CoV-2 was detected there — consistent with a systemic response to the virus.
Why is this research important?
This research shows that both mitochondrial energy production and organ health could be compromised in the long term after SARS-CoV-2 infection. However, researchers also discovered a potential new treatment target. SARS-CoV-2 boosts the activation of a regulatory molecule called miR-2392, which lowers the expression of energy-producing mitochondrial genes. Neutralizing miR-2392 may be able to stop the virus from hijacking energy production — and prevent serious complications from SARS-CoV-2 infection.
Where can I go to learn more?
- Chronic viral infections may influence the likelihood of developing Long COVID, and different chronic infections were associated with different Long COVID symptoms.
- Autopsies of patients with COVID-19 showed evidence of SARS-CoV-2 infection throughout the entire body, even among those who had mild or asymptomatic cases.
- In a study supported by the Researching COVID to Enhance Recovery (RECOVER) Initiative, researchers found that people from certain racial and ethnic groups are more likely than people from other groups to experience certain symptoms linked to Long COVID.
Guarnieri, J. W., Dybas, J. M., Fazelinia, H., Kim, M. S., Frere, J., Zhang Y., Albrecht, Y.S., Murdock, D. G., Angelin, A., Singh, L. N., Weiss, S. L., Best, S. M., Lott, M. T., Zhang, S., Cope, H., Zaksas, V., Butler-Saravia, A, Meydan, C., Foox, J., … Wallace, D. C. (2023). Core mitochondrial genes are down-regulated during SARS-CoV-2 infection of rodent and human hosts. Science Translational Medicine, 15(708), eabq1533. https://doi.org/10.1126/scitranslmed.abq1533
NIH COVID-19 Resources by Topic
COVID-19 research information and resources by topic from NIH institutes and centers