A simple explanation of how the new corona drug ``remdecibir'' works is like this

The Ebola drug

lemdecivir is believed to be effective as a treatment for new-type coronavirus infections (COVID-19), and in the United States on June 29, 2020, the price for developed country governments is $ 2340 per patient. It was announced that it was set to (about 250,000 yen). However, science writer Bruce Goldman said, 'Lemdesibir is not the ultimate coronavirus killer,' and explains how drugs work and their limitations.

How remdesivir works, and why it's not the ultimate coronavirus killer-Scope

The virus grows in the cells of the host while self-replicating, and the new coronavirus (SARS-CoV-2) enters the vesicles, which consist of biological membranes called endosomes , in the human body in the process. SARS-CoV-2 in the endosome is in a state of being wrapped in the viral membrane, but when it fuses with the cell membrane, its contents are effused into the cytosol . The content contains the viral genome, which creates thousands of identical genes within the cell membrane, eventually exploding the cell membrane and infecting more cells. Repeat the growth with.

The virus replicates one RNA, and there are two main methods: 'complete replication' and 'multiple partial replication'. The former is the seed of the virus itself that spreads the infection, while the latter is a fragment that conveys the method of virus production to the structure that makes cellular proteins called

ribosomes .

In order to virus makes a copy in any way polymerase that requires a protein that functions as a genetic material copy machine. All organisms replicate a DNA-based genome and require a polymerase to rewrite the gene into RNA-based instructions so that the ribosome can read it.

On the other hand, since the SARS-CoV-2 genome is made of RNA, it already has an affinity for ribosomes. Therefore, it is not necessary to rewrite DNA into RNA, but it is necessary to replicate RNA based on RNA, and SARS-CoV-2 lacks the polymerase for that purpose. However, the genome of SARS-CoV-2 has the gene code itself of RNA replication polymerase, and if it can catch ribosome, it is possible to produce a polymerase that actually functions from this code. As a result, the virus enters cells with 10 million ribosomes.

When a virus is able to make a polymerase, it not only makes more than one exact copy of the virus, it also increases the number of fragments that tell how to make it. This fragment tells the ribosome to make a protein that replicates the virus.

The newly produced protein contains many polymerases and is repeatedly fed to the SARS-CoV-2 genome. This makes it possible for the virus's original RNA to be replicated innumerably.

However, the polymerases that viruses make are slower than the polymerases that human cells make. For this reason, there are many errors and mutations in the RNA copy created. Coronavirus containing SARS-CoV-2 has a protein that corrects the above error, and it seems to cut the wrong chemical unit of RNA sequence and insert the correct one.

An antiviral drug that uses this mechanism is lemdecivir. Remdecibir masquerades as the 'correct chemical unit' for error correction and is incorporated into RNA sequences. An RNA copy with lemdecivir can either stall polymerase production or create defective polymerases. On the other hand, lemdecivir does not affect the polymerases produced by human cells.

Defective RNA copies do not allow SARS-CoV-2 to proliferate well and rupture the cell membrane to pop out, ultimately allowing the virus to fulfill its mission and recover the patient. However, because the escaped copy of lemdesibir can go out of the cell and spread the infection to other cells, lemdesibir is not a 'perfect medicine.'

It should be noted that, although no drug has been discovered that inhibits the protein that corrects the error in the virus, it is thought that lemdecivir can further increase its efficacy in combination with such a drug.

in Science, Posted by darkhorse_log