3 Existing Drugs Fight Coronavirus with ‘almost 100%’ Success

Israeli scientists say they have identified three existing drugs that have good prospects as COVID-19 treatments, reporting that they illustrated high ability to fight the virus in lab tests.

They placed the substances with live SARS‑CoV‑2 and human cells in vitro. The results “showed that the drugs can protect cells from onslaught by the virus with close to 100 percent effectiveness, meaning that almost 100% of the cells lived despite being infected by the virus,” Prof. Isaiah Arkin, the Hebrew University biochemist behind the research, told The Times of Israel.

By contrast, in normal circumstances, around half the cells would have died after two days following contact with the virus.” He added there are strong indications that the drugs will be robust against changing variants.

Arkin, part of a Hebrew University center that specializes in repurposing existing drugs, said that he screened more than 3,000 medicines for suitability, in what he describes as a needle-in-a-haystack search. This approach can provide a fast track to find treatments as the drugs have already been tried and tested, and he hopes to work with a pharmaceutical company to quickly get the medicines he identified clinically tested for COVID-19.

We have the vaccine, but we shouldn’t rest on our laurels, and I would like to see these drugs become part of the arsenal that we use to fight the coronavirus,” he said. When confronting SARS‑CoV‑2, the drugs in question — darapladib, which currently treats atherosclerosis; the cancer drug Flumatinib; and an HIV medicine — don’t target the spike protein. Rather, they target one of two other proteins: the envelope protein and the 3a protein. These proteins — especially the envelope proteinhardly change between variants, and even between diseases from the coronavirus family. As such, drugs that target them are likely to remain effective in spite of mutations, Arkin said.

Source: https://www.timesofisrael.com/

Coronavirus And Cancer Hijack The Same Parts In Human Cells To Spread

Most antivirals in use today target parts of an invading virus itself. Unfortunately, SARS-CoV-2 – the virus that causes COVID-19 – has proven hard to kill. But viruses rely on cellular mechanisms in human cells to help them spread, so it should be possible to change an aspect of a person’s body to prevent that and slow down the virus enough to allow the immune system to fight the invader off.
A  quantitative biologist built a map of how the coronavirus uses human cells.  He used that map to find already existing drugs that could be repurposed to fight COVID-19 and has been working with an international group of researchers called the QBI Coronavirus Research Group to see if the identified drugs showed any promise. Many have.

For years, researchers have suspected that kinases – biological control switches that viruses use to take over cells – could be targeted to fight infections. Over the last few months, we built a second, more detailed map looking specifically for the kinases that the coronavirus is hijacking.

A few already existing cancer drugs have been identified which alter the function of the kinases that SARS-CoV-2 hijacks, and began testing them in coronavirus-infected cells. The results of these early tests are promising  and human clinical trials have begun.

 

This map shows how the coronavirus changes the function of kinases – cellular switches involved in most biological processes – and the proteins they control. It guided researchers from UCSF to cancer drugs that could fight COVID-19. 

 

Kinases are proteins found in every cell of our body. There are 518 human kinases, and they act as major control hubs for virtually all processes in the body. They are able to add a small marker – a process called phosphorylation – to other proteins and thus change how, if and when a phosphorylated protein can do its work.

Source: https://theconversation.com/

CRISPR Reverses Duchenne Muscular Dystrophy Mutation

CRISPR-Cas9 has, for the first time, been tested by systemic delivery in a large animal—and the results are striking. Working in a dog model of Duchenne muscular dystrophy (DMD), the gene editing not only restored the expression of the protein dystrophin, it also improved muscle histology in the dogs.

Our technology was developed using human cells and mice to correct the same type of mutation as in these dogs. It was critical for us to test gene editing in a large animal because it harbors a mutation analogous to the most common mutation in DMD patients,” said Eric Olson, Ph.D., professor and chair of molecular biology at the University of Texas Southwestern Medical Center and lead author. The researchers wrote that this is “an essential step toward clinical translation of gene editing as a therapeutic strategy for DMD.”

Indeed, Dame Kay E. Davies, Ph.D., professor of anatomy and director of the MRC Functional Genomics Unit at the University of Oxford and a pioneer in the field of DMD research, echoes this sentiment explains, “This is a very exciting paper as it shows that gene editing can be reasonably affective in a large animal model of DMD.”

The paper, “Gene editing restores dystrophin expression in a canine model of Duchenne muscular dystrophy,” appears in the last issue of Science.

Source: https://www.genengnews.com/