A consortium of researchers, including those from the Children’s Hospital of Philadelphia (CHOP) and the COVID-19 International Research Team (COV-IRT), has found that the SARS-CoV-2 virus can adversely affect mitochondrial genes. This leads to dysfunction in various organs other than the lungs, signifying that COVID-19 should be perceived as a disorder affecting the whole body. The discovery opens new avenues for treatment, specifically focusing on microRNA 2392.
Though the lungs’ mitochondrial function appeared to recover, the same was not observed in the heart and other organs. This ongoing damage could shed light on the negative long-term effects known as “long COVID.”
Since the beginning of the COVID-19 pandemic, researchers have been examining the distinctive prolonged effects of this virus compared to other coronaviruses.
The study found that the virus can negatively influence mitochondrial genes—the cell’s energy producers—causing multiple organ dysfunction, not just in the lungs. These findings, published in Science Translational Medicine, lay the groundwork for innovative COVID-19 treatments.
Mitochondria are present in all our cells, with genes responsible for creating them dispersed across both nuclear and mitochondrial DNA (mtDNA). Earlier research indicated that SARS-CoV-2 proteins might bind to mitochondrial proteins, potentially resulting in dysfunction.
The researchers from the Center for Mitochondrial and Epigenomic Medicine (CMEM) at CHOP, along with COV-IRT, analyzed mitochondrial gene expression using various tissue samples and animal models to identify the differences induced by the virus.
In the study’s autopsy tissue, the lungs showed recovered mitochondrial gene expression, but this recovery was not seen in the heart, kidneys, liver, or even the cerebellum, despite no SARS-CoV-2 in the brain. Additional animal models indicated recovery of mitochondrial function in the lungs during the infection’s mid-phase.
These findings demonstrate that the initial infection response involves the lungs, but eventually, mitochondrial function in the lungs improves, while in other organs, especially the heart, it remains hindered.
Co-senior author Douglas C. Wallace, Ph.D., emphasized the necessity to view COVID-19 as a systemic disorder affecting various organs, with persistent dysfunction in organs other than the lungs potentially causing long-lasting damage.
The study also uncovered potential therapeutic targets, such as microRNA 2392 (miR-2392), known to regulate mitochondrial function. This could offer an additional treatment option for those at risk of more severe complications.
Earlier, funding from The Gates Foundation supported research into how variations in mtDNA among global populations might influence mitochondrial function and sensitivity to SARS-CoV-2. Wallace indicated that the clear impact of SARS-CoV-2 on mitochondrial function supports the idea that individual variations in mitochondrial function could play a role in the severity of COVID-19.
This research was also supported by the Division of Intramural Research, NIAID, NIH, and partially by the Bill & Melinda Gates Foundation grant INV-046722. The study was published on 9 August 2023 in Science Translational Medicine, DOI: 10.1126/scitranslmed.abq1533.
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Frequently Asked Questions (FAQs) about fokus keyword: mitochondrial dysfunction
What did the researchers discover about COVID-19’s impact on organs?
Researchers found that the SARS-CoV-2 virus can negatively affect mitochondrial genes, leading to dysfunction in various organs beyond the lungs. The discovery redefines COVID-19 as a systemic disorder and opens up new avenues for treatment, including targeting microRNA 2392.
How does SARS-CoV-2 affect mitochondrial function?
The virus can adversely affect the genes of mitochondria, which are the energy producers in cells. This leads to dysfunction in several organs, not just the lungs. Earlier studies also showed that SARS-CoV-2 proteins might bind to mitochondrial proteins, potentially causing dysfunction.
What is the significance of mitochondrial dysfunction in the context of COVID-19?
The dysfunction in mitochondrial genes caused by the SARS-CoV-2 virus has been linked to long-term damage in multiple organs, including the heart, kidneys, and liver. This might provide an explanation for the adverse effects associated with “long COVID” and emphasizes the need to treat COVID-19 as a disorder that impacts the entire body.
Have the researchers identified any potential therapeutic targets?
Yes, the research team found a potential therapeutic target in microRNA 2392 (miR-2392), which was shown to regulate mitochondrial function in human tissue samples. Neutralizing this microRNA might impede the replication of the virus, providing an additional treatment option for patients at risk of more severe complications.
Who supported and funded this research?
This work was supported by the Division of Intramural Research, NIAID, NIH, and in part by the Bill & Melinda Gates Foundation grant INV-046722. The research was also conducted by a consortium including the Children’s Hospital of Philadelphia (CHOP) and the COVID-19 International Research Team (COV-IRT).
Where was the study published?
The study was published in the journal Science Translational Medicine on 9 August 2023, with the DOI: 10.1126/scitranslmed.abq1533.
5 comments
Wow, this is eye-opening stuff! never knew that COVID could affect so many organs. We need to get this information out to more ppl!
Always wondered why COVID was hitting some people so hard. This might be the answer we’re looking for, finally. Lets hope for more progress.
This is huge, a real game changer for treating covid! that miR-2392 thing, i hope they can make a treatment from it soon.
I don’t really understand all this science stuff, but it sounds like they are finding more ways to help people with COVID. which is great news.
What does this mean for long term treatments? Can they fix the mitochondria or is this permanent damage? Really worried about my uncle who’s been struggling with long covid 🙁