Covid Symptoms Prevented by New Drug Used on Mice, No Risk of Resistance

Research findings from new studies show that organ damage resulting from Covid-19 can be averted by an antioxidant enzyme that shields a cell’s mitochondria. The study was led by a devoted team of scientists from CHOP (Children’s Hospital of Philadelphia) and was discussed by them in an article recently published. The compound that formed the basis for their research, EUK8, served two functions. First, it prevented the mice that it was tested on from becoming severely ill, with the symptoms of Covid-19 not registering to the same extent in them. Secondly, it inhibited the production of mitochondrial reactive oxygen species (mROS), which causes organ damage through inflammation.

This team was previously part of a group that showed the causative link between organ dysfunction and the mitochondria in patients who were severely sick with Covid-19. Those studies concluded that SARS-CoV-2 inhibited the mitochondrial genes responsible for mitochondrial oxidative phosphorylation (OXPHOS), thus limiting cellular energy production. Furthermore, it induces cells to make the molecules that allow the virus to replicate and thereby spread. This is achieved by increasing mROS levels, leading to harmful inflammation as a result.

The evidence collected to support these findings was present in the bodies of people who had died from Covid-19. The suppression of mitochondrial genes was no longer an issue in the lung samples collected, but in other parts of the body, this suppression could still be seen, leading to the conclusion that there was long-term damage.

The current study involved an experiment on 12-week-old mice. The purpose was to investigate whether the virus could be stopped from affecting OXPHOS by limiting mROS levels with the new compound, EUK8. The latter is a catalytic antioxidant which, as the name suggests, would counteract the virus by breaking down compounds associated with oxidative stress, like mROS.

The mice were divided into three groups and given one of three treatments. One group was given MitoCocktail, which proposed to boost OXPHOS levels. The second group was given EUK8, the subject of this research. The third group was given both. The researchers, in comparing the treatments, aimed to find out what the most efficacious strategy would be: boosting OXPHOS or reducing mROS levels. Another group of mice formed the control group. As part of the experiment, the researchers were blind to the treatments given.

One day after receiving the treatment, the mice were infected with SARS-CoV-2. On the fifth day after being infected, those who had received the EUK8 treatment showed lower weight loss than other mice from any group. They also had lower levels of inflammation, viral proteins, and impaired OXPHOS.

The conclusion drawn from this study was that reducing mROS, rather than increasing OXPHOS, helped combat mitochondrial damage stemming from Covid-19 most effectively. This was reported by Douglas Wallace, a Ph.D. on the research team, who said in a press release, “We believe that reducing mROS represents a superior strategy for mitigating the pathogenicity of SARS-CoV-2.”

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