Researchers from the Hebrew University and Mount Sinai Hospital in New York cracked the replication mechanism of the corona virus and found an existing drug that attacks it

Prof. Jacob Nahmias, head of the Center for Bioengineering at the Hebrew University, in collaboration with Mount Sinai Hospital in New York, discovered that the SARS-CoV-2 virus causes the accumulation of fat in lung cells in order to replicate itself. A drug for the treatment of excess lipids in the blood approved by the FDA was able to suppress the activity of the virus in a laboratory experiment and stop its spread

The action of the drug fenofibrate against the corona virus. Photo: Prof. Kobi Nachmias
The action of the drug fenofibrate against the corona virus. Photo: Prof. Kobi Nachmias

Viruses do not have the basic tools necessary for replication, and must use the metabolic mechanisms of host cells to reproduce and complete their life cycle. Understanding how parasites such as the new corona virus SARS-CoV-2 changes the metabolism of lung cells may help us explain why the morbidity rates in the corona disease COVID-19 are high and help identify a new drug that blocks the replication of the virus or limits the progression of the disease. Prof. Yaakov Nahmias, head of the Center for Bioengineering at the Hebrew University, was able to track the changes caused by the corona virus in lung cells, and even find an existing drug that is already approved for use and can neutralize the activity of the virus.

During the last few months, while most of the country was under quarantine, the computers in Prof. Nachmias' laboratory began working on new information that came from Mount Sinai Hospital in New York State. "We knew that we had tools that no one else had," said Prof. Nachmias, "and based on the new information, we began to scan for the ways of the virus in our robotic system."

The collaboration between Prof. Nachmias and Prof. Benjamin Tanover from Mount Sinai Hospital in New York led to a significant breakthrough in understanding the ways of operation of the SARS-CoV-2 virus. The researchers found that the virus causes a massive accumulation of fat in human lung cells after it rewires the cell's metabolic mechanisms. Prof. Nachmias' robotic scanning system showed that lung cells infected with the virus consumed more carbohydrates, such as glucose, which are needed for the rapid division of the virus, and created fats from them that gradually accumulated in the lung tissue. These findings explain why high blood sugar (hyperglycemia) and high cholesterol (dyslipidemia) are a major risk factor for corona, even in the absence of diabetes.

The laboratory of Prof. Kobi Nachmias. Photo: Daniel Hanoch
The laboratory of Prof. Kobi Nachmias. Photo: Daniel Hanoch

Prof. Nachmias: "Our analysis is the first comprehensive description of the human lung response to the SARS-CoV-2 virus. We show that the lung response to SARS-CoV-2 is primarily metabolic, and leads to lipid accumulation in the lung. Our data indicate that lipid accumulation Abnormality May Underpin Critical Aspects of COVID-19 Development This is a breakthrough that opens up possibilities for neutralizing the virus' action through activity targeting The host tissue that allows it a substrate to develop. This led us to check which existing drugs can impair the ability of the virus to replicate itself and curb the severity of the disease."

Prof. Nachmias was able to find a drug called fenofibrate (Ticor) which was already approved in 1975 by the FDA. Fenofibrate was previously used to treat high levels of cholesterol and triglycerides in the blood, and has since been replaced by statins. In a laboratory experiment, fenofibrate allowed lung cells to break down the lipids quickly and block the ability of the corona virus to "hijack" the metabolism of my cells lung, thus actively suppressing its replication - and as a result, also the development of the disease.

Prof. Nahmias: "Our discovery came just in time, because there are new indications that suggest that vaccines being developed today may only protect patients for a few months. On the other hand, if our results are confirmed in a clinical study, drug treatment could within a few months turn COVID- 19 for a type of cold." "The collaboration between Prof. Nachmias and TenOever Laboratories demonstrates the power of adopting a multidisciplinary approach to SARS-CoV-2 research," added Prof. Benjamin Tenover, Prof. Nachmias' research partner from Mount Sinai Hospital in New York, "Our findings really may significantly reduce the global burden of COVID-19."

Prof. Kobi Nahmias. Photo: Daniel Hanoch.
Prof. Kobi Nahmias. Photo: Daniel Hanoch.

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7 תגובות

  1. Unfortunately, this looks like advertising on behalf of certain politicians who are failing to take real action against the corona virus. At such a stage, other researchers refrain from publishing, because the chances that the drug will actually succeed are very low. And publishing in non-scientific newspapers at such a stage is something that can destroy a career.

  2. Sounds good and therefore looks good, like all studies dealing with the virus.

    Let's hope that this time it really is a breakthrough that can quickly bring us closer to the long-awaited vaccine, and of course to an effective vaccine.

  3. Was the study published in some peer-reviewed journal, or is this another one of those promises that are thrown into the air twice a week?

  4. It is enough to eliminate sugar-protein chopsticks for him.

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