UK Prime Minister Boris Johnson recently announced the creation of an anti-virus task force to “push” the development of new antiviral drugs.
At a press conference in Downing Street, Johnson said: “The majority of scientific opinion in this country remains firmly convinced that there will be another wave of COVID sometime this year.”
The prime minister hopes to have antiviral drugs available in the fall to help quell this third wave.
While there are anti-inflammatory medications that reduce the risk of death from COVID, such as dexamethasone and tocilizumab, these they are only given to people hospitalized with severe COVID.
But Johnson wants drugs that can be taken at home, in pill form, that prevent people from ending up in the hospital on a ventilator.
As usual, new antiviral drugs take years to develop and approve because the discovery process involves painstaking work identifying chemical compounds that attack the virus and then testing their efficacy and safety.
For this reason, scientists are also studying the possibility of repurposing existing drugs that have been approved to treat other viruses or diseases.
Unlike broad-spectrum antibiotics, which can be used to treat a wide range of bacterial infections, drugs that work against one type of virus rarely work to treat other viruses.
For example, remdesivir, originally developed for the treatment of hepatitis C, was once suggested as a treatment for COVID, but clinical trials have shown that it has only a limited effect against this coronavirus.
The reason there are few effective broad-spectrum antivirals is that viruses they are much more diverse than bacteriaeven in the way they store your genetic information (some in the form of DNA and others as RNA).
Unlike bacteria, viruses have fewer protein components of their own that can be attacked with drugs.
For a drug to work, it has to reach its goal.
This is particularly difficult with viruses because they replicate within human cells by hijacking our cellular machinery.
The drug must penetrate infected cells and act on processes that are essential for the normal functioning of the human body.
Unsurprisingly, this often results in collateral damage to human cells, experienced as side effects.
Targeting viruses outside of cells, to prevent them from taking hold before they can replicate, is possible, but is also difficult due to the nature of the virus envelope.
The viral envelope is extraordinarily robust, resistant to the negative effects of the environment he faces on the way to his host.
Only then does it decompose or eject its content, which contains your genetic information.
This process can be a weak point in the life cycle of the virus, but the conditions that are controlled by the release are very specific.
While drugs that target the virus envelope seem attractive, some can still be toxic to humans.
It is hard but not impossible
Despite these difficulties, drugs have been developed to treat viruses such as influenza and HIV.
Some of these drugs target viral replication processes and viral envelope assembly.
But developing new drugs takes a long time, and viruses mutate quickly.
So even when a drug is developed, the ever-evolving virus you could soon develop resistance to the drug.
Another problem in fighting viruses is that several of them, such as HIV, papillomavirus, and herpes, can remain dormant.
In this state, the infected cells do not produce any new virus. The genetic information of the virus is the only viral thing present in cells.
Medications that interfere with the replication or envelope of the virus have nothing to act against, so the virus survives.
When the sleeping virus becomes active again, symptoms are likely to reappear and therefore further treatment with a drug is necessary.
This increases the possibility of drug resistance developing as the virus undergoes drug-induced selection for resistant variants longer.
Although we are still beginning to understand the life cycle of coronaviruses, there are indications that they may persist for a long time, particularly in patients with weak immunity, resulting in the additional problem of creating more resistant virus strains.
Research to understand how the coronavirus works has come a long way in a short time, but when it comes to developing antivirals, many questions remain to be answered.
With the possible resurgence of infections expected by the end of the year, the antiviral task force has a lot of work ahead of it.
* Pavol Bardy is a research associate of structural virology at the University of York, Fred Anston is a professor of chemistry at the University of York, and Oliver Bayfield is a research associate in chemistry at the University of York.
This article originally appeared on The Conversation. You can read the version original and see links to scientific studies here.
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Eddie is an Australian news reporter with over 9 years in the industry and has published on Forbes and tech crunch.