The research examined some of the critical differences between how acute coronavirus 2 (SARS-CoV-2) respiratory syndrome and other viruses affect mitochondrial genes, as the -differences between them help provide answers as to why some older adults and people with metabolic disorders have more severe responses to COVID-19 than others. In addition, such investigations can help to provide a starting point for identifying treatment.
“If you already have mitochondrial and metabolic dysfunction, it is possible that, as a result, you have a first line of defense against COVID-19. Future work should consider mitochondrial biology as a primary target. intervention for SARS-CoV-2 and other coronaviruses, “lead author Pinchas Cohen, MD, professor of gerontology, medicine and biological sciences and dean of USC ‘s Leonard Davis School, said in a press release.
The findings of the research also helped to show how COVID-19 removes mitochondrial genes from their normal function to modulate the body’s natural response.
“We already knew that our immune response was not successfully upgrading to COVID-19, but we didn’t know why,” lead author Brendan Miller, a senior doctoral student at USC’s Leonard Davis School, said in press release. “What we did differently is look at how the virus specifically targets mitochondria, a cellular organelle that is a vital part of the body’s immune system and energy production.”
In conducting the research, the team performed ribonucleic acid (RNA) sedation analyzes that compared mitochondrial-COVID-19 interactions with 3 other viruses, which included respiratory syncytial virus. , seasonal influenza A virus, and human parainfluenza virus 3.
The results of the analysis showed that there are 3 ways that COVID-19 suppresses the body’s cellular immune response in a way that is different from other viruses. In particular, they found that SARS-CoV-2 reduces complex I levels, which are a group of mitochondrial proteins encoded by nuclear DNA.
The researchers maintained that by reducing complex I levels, cell metabolic production and the generation of reactive oxygen species could be silenced, which would in turn limit the inflammatory response virus.
“COVID-19 reprogramns the cell so that they do not make these complex proteins associated with I. That could be one way in which the virus spreads,” Miller said in the press release, noting, however, that these findings still need to be confirmed future research.
In addition, the research showed that SARS-CoV-2 does not affect messenger protein levels, mitochondrial antiviral protein messenger RNA, which is a protein responsible for cell communication that a viral attack has occurred. Typically, when this protein is activated, it acts as a warning system that warns the cell to self-destruct to stop the virus from reproducing.
Also, the researchers noted that genes encoded by mitochondria did not get on or off with SARS-CoV-2. This process of turning on and off to generate energy that will help the cell to attack a virus is currently understood.
“This study contributes to a growing body of research on mitochondrial-COVID-19 interactions and demonstrates stress and cell-specific effects that should be carefully considered in future trials, “Cohen said in the press release.
REFERENCE
New findings will help explain how COVID-19 is gaining the upper hand over the immune system. Los Angeles, CA: University of Southern California; 8 January 2021. eurekalert.org/pub_releases/2021-01/uosc-nfh010821.php. Accessed 11 January 2021.