Coronavirus treatments: what drugs might work against COVID-19?

As the COVID-19 pandemic continues to spread across the world, killing thousands and bringing economies to their knees, doctors, scientists and governments are on the lookout for safe and effective treatments to help those who are sick. And yet a large issue with COVID-19 is that there is, as yet, no cure.

Though there are treatments that can alleviate the symptoms – such as difficulty breathing – they do not address the underlying cause: the virus. The idea is that treating the symptoms will help prolong a patient’s life and buy time for their own immune systems to kick in and remove the infection.

While research into related coronaviruses over the last few decades has brought some promising looking drugs, only large clinical trials on patients with COVID-19 will be able to reveal precisely whether these interventions are safe and effective. Unfortunately, these kinds of large trials take time to carry out, but they are ongoing.

The World Heath Organization (WHO) announced it has helped to launch four “mega trials” against COVID-19 and there are countless more smaller ones coordinated in countries worldwide.

The WHO-backed trials are focusing on drugs that are thought to directly block SARS-CoV-2 – the virus strain that causes coronavirus COVID-19 – from replicating inside our lungs. Below are some of the main drugs these trials are looking at.

Remdesivir
This is an intravenous antiviral drug that was developed to block infection with related coronaviruses and even Ebola, and is one of the drugs the WHO is helping to investigate.

Remdisivir has already been shown to work against SARS-CoV-2 in cells in a dish in a lab as well as in mice infected with the virus. Remdesivir specifically targets key viral proteins involved in making new copies of the virus and prevents them from working.

Remdesivir has already been used in some COVID-19 patients in the US and appears safe, but large trials are needed to really know if this is the case.

This is a drug combination used against viruses like HIV. It works in a similar way to remdesivir by blocking key viral proteins called “proteases”.

Lopinavir/ritonavir has also been shown to be effective against SARS-CoV-2 in lab cells as well as in mice and is being tested alongside an antiviral drug called interferon beta. This is currently used to treat Multiple sclerosis and can enhance the natural defences of the body’s cells against COVID-19.
Chloroquine and hydroxychloroquine

Both of these drugs are currently used to treat malaria and the autoimmune disease lupus. 

Chloroquine has been tested against lots of different infections because in the lab it can block viruses – including SARS-CoV-2 - from getting inside cells placed in a dish and so prevent infection.

Outside the lab, chloroquine has not been demonstrated to have a profound effect at preventing disease and there is limited evidence so far that it can work for COVID-19, despite receiving a lot of hype from President Donald Trump. But again, large trials are needed and the WHO is supporting these.

Caution should be observed with chloroquine as it can have significant side effects in certain people and may even block the immune response – the desired result in lupus treatment.
Two other options

The above potential treatments all work by blocking some key element of the virus infection machinery using small molecules. Two other kinds of treatments are also being explored in trials that work in a different way.

The first is passive immunisation which is the transfer – or transfusion – of potential protective antibodies from someone who has been infected and recovered from COVID-19 to someone who is at high-risk or is suffering from a SARS-CoV-2 infection.

This so-called “convalescent sera” (which is a purified blood product from someone who has recovered from COVID-19) can block SARS-CoV-2 in cells in a dish in the lab and has the potential to help develop treatments. Passive immunisation for COVID-19 is being tested in trials across the world and so far results seem to suggest it is safe to use.

Another kind of possible treatment works by blocking parts of our own immune system that are likely overreacting to SARS-CoV-2 infection and contributing to the damage in our lungs.

In the limited studies that have been conducted on COVID-19, it seems that in some severe cases our immune response goes into overdrive without being able to clear the infection and this can increase the severity of the disease. When this happens, high levels of inflammation is found in the lungs.

Potential treatments that look at blocking the immune components linked to this severity have begun. That said, extreme caution must be taken when manipulating the immune response during an infection as in the absence of other therapies we rely on our immune response to limit the virus replicating.

So although specific treatments for COVID-19 are not yet available, drugs are being tested and clinical trials and starting to yield results. This, combined with the further knowledge that scientists are gaining about SARS-CoV-2 will help massively until a vaccine becomes available.

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Anti-malaria drugs help in treating cancer

According to previous researches, anti-malaria drugs known as chloroquines were repurposed to treat cancer for decades, but until now no one knew exactly what the chloroquines were targeting when they attack a tumor.
 
Now, researchers  explained that an enzyme called PPT1 - opens up a new pathway for potential cancer treatments. 

The team also used CRISPR/Cas9 gene editing to remove PPT1 from cancer cells in the lab and found that eliminating it slows tumor growth. They detailed a potent chloroquine, known as DC661, that can take advantage of this new treatment pathway.

"The discovery of this target is critical because chloroquines are currently being evaluated in clinical trials all over the world, and this knowledge fundamentally changes the way we look at those trials," said the study's co-senior author.

PPT1 is an enzyme which helps in controlling both the mechanistic target of rapamycin (mTOR), a major regulator of growth in cancer cells, as well as a process called autophagy, a built-in resistance mechanism which allows cells to survive when under attack by breaking down unneeded parts and recycling them to stay alive.
In a previous study, researchers showed these two processes work hand-in-hand, as autophagy provides the nutrients that allow mTOR to direct growth, while mTOR shuts off autophagy when the nutrients aren't needed.

Building off their previous work, researchers used CRISPR/Cas9 to knockout PPT1 from cancer cells to see if its removal had the same effect as a chloroquine.

Researchers further proved that the concept by targeting melanoma cells with DC661, which specifically targets PPT1 and produces cell death in many cell lines tested both in vitro and in vivo. It is a dimeric form of the antimalarial drug quinacrine - meaning it has two molecules of quinacrine bound together with a special linker.
The researcher added that when you put the pieces together, it shows incredible promise.

"We now have a specific molecular target in cancer, as well as a potent way to reach it," he said. "It not only provides a new context for current clinical trials involving hydroxychloroquine but also, with further development of these compounds toward clinical drug candidates, it opens the door for head-to-head testing of our compounds or their optimized derivatives versus current chloroquines to see which is more effective." 

 

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Innovative method to fight malaria

An anti-malarial treatment that lost its status as the leading weapon against the deadly disease could be given a new lease of life, with new research indicating it simply needs to be administered differently.

The findings could revive the use of the cheap anti-malarial drug chloroquine in treating and preventing the mosquito-borne disease, which claims the lives of more than half a million people each year around the world, DECCAN Chronicle reported.

The parasite that causes malaria has developed resistance to chloroquine, but research carried out at the Australian National University (ANU) and Germany's University of Heidelberg has shown that the parasite protein that causes resistance has an Achilles' heel. 

"We studied diverse versions of this protein and in all cases found that it is limited in its capacity to remove the drug from the parasite," said malaria researcher Dr Rowena Martin.

"This means malaria could once again be treated with chloroquine if it is administered twice-daily, rather than just once a day," said Martin. Once hailed as a wonder drug, chloroquine is still used in developing nations in the South Pacific, Africa, Asia and South America , but has been withdrawn from use in many developed countries. 

Martin and her colleagues also revealed how the protein may have developed resistance to chloroquine. "We found that the protein gains the ability to move chloroquine out of the parasite through one of two evolutionary pathways, but that this process is rigid one wrong turn and the protein is rendered useless," she said. 

"This indicates that the protein is under conflicting pressures, which is a weakness that could be exploited in future antimalarial strategies," said Martin. Martin said the findings could be used to help millions of people in developing nations who are at risk of catching malaria.

She said that there is also potential to apply the findings to several chloroquine-like drugs that are also becoming less effective as the malaria parasite builds up resistance.

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