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Experts explain why the SARS-CoV-2 virus is so difficult to treat

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Kamal Saini
Kamal S. has been Journalist and Writer for Business, Hardware and Gadgets at Revyuh.com since 2018. He deals with B2b, Funding, Blockchain, Law, IT security, privacy, surveillance, digital self-defense and network policy. As part of his studies of political science, sociology and law, he researched the impact of technology on human coexistence. Email: kamal (at) revyuh (dot) com

The research unexpectedly brings new insight into the immune response to coronavirus infections, could help to find better treatments for COVID-19.

An international team of researchers has figured out the reason for the slow and difficult recovery after a severe course of coronavirus infection.

The research, published this week in the journal Science Immunology, proposes that the pairing of antiviral drugs with drugs that inhibit this process may be more effective to treat COVID-19.

The results of the study found that SARS-CoV-2 triggers the activation of the recently discovered immune complement system in lung cells – anti-pathogenic defense regulated by the liver. Moreover, it directs it against the body’s own cells.

Scientists have found that the immune complement system – a collection of certain proteins produced by the liver to fight pathogens transmitted through the blood – can work inside cells, and not just in the bloodstream.

It turned out that the immune complement system is triggered in the alveoli – small structures of the lungs through which gas exchange takes place.

“We observed that SARS-CoV2 infection of these lung cells causes expression of an activated complement system in an unprecedented way. This was completely unexpected to us because we were not thinking about activation of this system inside the cells, or at least not lung cells. We typically think of the complement source as the liver,” commented the co-author of the work, Majid Kazemian, on the results.

The complement system, derived from the liver and bloodstream, protects the host from infections caused by bacteria, viruses, and fungi, he said. In the presence of SARS-CoV-2, it turns against it and promotes tissue inflammation, experiments have shown.

“These findings provide important evidence showing not only that complement-related genes are amongst the most significant pathways induced by SARS-CoV2 in infected cells, but also that activation of complement occurs inside of lung epithelial cells, i.e., locally where infection is present,” says Dr. Ben Afzali from National Institute of Health’s National Institute of Diabetes and Digestive and Kidney Diseases.  

This, according to the scientist, explains the reason for the lack of effectiveness of treatment, which targets the complement system outside the cells and in the bloodstream.

“We should probably consider using inhibitors of complement gene transcription or complement protein activation that are cell permeable and act intracellularly instead,” he further explained.

The research was published last week in the journal Science Immunology.

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