London - Modern science has scarcely presented a more crucial goal, offering untold riches and perhaps even a Nobel prize to the victor, as well as the chance to return the world to normal.
Yet the search for a cure for coronavirus is also uniquely perilous thanks to the dangers inherent in rushing new medical products to market.
Across the globe, thousands of researchers employed by governments, laboratories and drug firms are working flat-out to crack this all-important riddle.
As are endless armchair experts, whose numbers now evidently include Donald Trump.
Yesterday, the world’s most powerful man used a press conference to propose various highly unorthodox new treatments for coronavirus, including ‘injecting’ disinfectant into the body and blasting patients with ultraviolet light.
Back in the real world, researchers are working tirelessly to combat the virus.
But while bullish claims have been made for a host of possible treatments, the truth is that scientists have little idea which ones might end up being of use.
‘Four months into the pandemic, we have had millions of people infected but no data yet to show that any particular treatment is especially effective,’ says Professor Babak Javid, the Principal Investigator at Tsinghua University school of medicine in Beijing, and a consultant in infectious diseases at Cambridge University Hospitals.
Nonetheless, here are some of the most likely candidates.
In mid-March, the American President used Twitter to amplify reports that Covid-19 patients could be successfully treated via a combination of the malaria drug hydroxychloroquine and a common antibiotic, Azithromycin.
In a later press conference, the President insisted that ‘common sense’ qualified him to make such a claim, urging Americans to ‘take it’ and asking them: ‘What have you got to lose?’
Well, quite a lot, as it turned out. The drugs have a catalogue of nasty side-effects, including an increased risk of cardiac arrest, skin blistering, hearing loss and an ‘inability to move the eyes’.
A study this week of 368 male coronavirus patients found that 28 per cent of those treated via hydroxychloroquine alone and 22 per cent who received both drugs (the malaria treatment and azithromycin) in U.S. hospitals died. This compares to a death rate of just 11 per cent for patients who received standard care without either drug.
Hope and hype about the drug Remdesivir have set Californian biotech firm Gilead’s share price soaring in recent weeks.
The medicine, which is administered via a drip, was originally developed to fight the ebola virus and works by interfering with its genetic makeup.
Although other drugs were soon found to be more effective at treating ebola, subsequent tests suggested Remdesivir had some effect on respiratory viruses such as Sars and Mers. It also appears to be relatively safe.
Gilead has so far given Remdesivir to 1,700 coronavirus patients, with dramatic effects reported in some cases. Two major studies, in the U.S. and Europe, are currently underway.
Sadly, a full-scale clinical trial in China, which has been running for longer, found no evidence it improved the fate of hospital patients, according to documents accidentally leaked this week by the World Health Organisation.
Gilead responded that these leaks contained ‘inappropriate characterisations’ and insisted their findings were ‘inconclusive’.
One reason that the Chinese trial’s outcome was so disappointing could be that Remdesivir is likely to work best if administered early.
‘With Covid-19, the virus mostly replicates soon after infection,’ says Professor Javid. ‘If you give the anti-viral later in the course of an illness, when a patient is hospitalised, there is not much virus left for the drug to attack.’
The ‘golden goose’ for pharmaceutical firms is to discover a new ‘antibody treatment’ that can attach to individual particles of coronavirus and stop them wreaking havoc.
Two US drug companies, Amgen and Adaptive, recently announced a partnership to study recovered Covid-19 patients in an effort to identify and manufacture crucial virus-killing antibodies.
Another firm, Regeneron, has been conducting a study using the virus’s genetic material in mice. Dozens of other companies are pursuing similar projects.
Although an antibody strategy was used against ebola, most new drugs take more than five years to develop, thanks — among other things — to rigorous testing designed to ensure they do not have dangerous side-effects.
This fashionable, if highly experimental, field involves harvesting blood from people who have recently recovered from coronavirus and donating it to patients who are still suffering from the disease.
Because blood plasma contains antibodies that have ‘learned’ how to detect and destroy the virus, the theory is that a transfusion will kick-start the recipient’s ability to fight it.
‘It’s quite easy to harvest plasma from surviving patients,’ says Professor Javid. ‘It was done even during the Spanish Flu epidemic of 1918-19.’
About 600 patients in America have already received this treatment. The NHS is also said to be preparing to carry out an extensive trial in the UK.
However, some experts have pointed out that many Covid-19 victims die because of an overactive immune response to the virus, causing inflammation of lungs and other vital organs. These experts worry that boosting a patient’s immunity via plasma therapy could actually worsen their condition.
Another problem with plasma therapy is the old-fashioned issue of supply and demand. A limited number of recovered patients are prepared to give blood, and only a finite amount can be taken from them.
However, technology now exists to manufacture synthetic antibodies using the blood of Covid-19 survivors’.
Such ‘monoclonal antibodies’ have become the standard treatment for ebola. Several laboratories have identified monoclonal antibodies that can apparently inhibit coronavirus in test-tubes.
Professor Javid warns, however: ‘No one has yet worked out which of the promising monoclonal antibodies work best for Covid-19, or what might be the best way to use them in combination. This is why they are not in production yet for Covid-19.’
Contracting HIV was once a virtual death sentence, but after decades of research, it’s now mostly a highly manageable condition thanks to a raft of well-tolerated drugs.
Indeed, many HIV drugs are now being touted as possible treatments for coronavirus, including Lopinavir and Ritonavir.
These are being trialled on coronavirus patients in studies at the Universities of Oxford and Nebraska.
But so far there is little evidence of them working outside of a laboratory setting.
The so-called ‘master cells’ that develop into blood, brain, bones and organs have been touted as the basis for cures for cancer, heart disease and arthritis for years.
Little wonder, then, that the pioneering field of stem cell therapy is now being targeted at coronavirus. Among firms exploring this modish area are Mesoblast, whose boffins are testing bone-marrow cells to establish whether they can help patients develop immunity to the virus. In Wuhan, meanwhile, doctor Dongcheng Wu last month claimed he’d treated nine patients by injecting umbilical stem cells. He said they all made a complete recovery within days. The success has not yet been convincingly replicated, however. Stem cell treatments are often risky, too — when trialled on Parkinson’s, they caused brain tumours.
Around half the patients who die with coronavirus suffer a so-called ‘cytokine storm,’ in which their immune system goes into overdrive, causing, among other things, acute lung inflammation that stops them from taking on enough oxygen. With this in mind, many products designed to combat inflammation are now being trialled on Covid patients.
They include Tocilizumab, used to treat rheumatoid arthritis, and Dexamethasone, a steroid used against asthma.
The World Health Organisation’s Solidarity trial is meanwhile testing interferon-beta, which is used to treat multiple sclerosis.
Professor Javid believes immune drugs should be accompanied by effective antiviral treatment: ‘We know from treating flu patients suffering cytokine storms that if you dampen their immune response without also giving them an antiviral drug, it can reduce the patient’s virus-fighting defences and allow the virus to run wild.’
These are the cholesterol-lowering drugs prescribed to millions at risk of heart disease. Now scientists wonder if statins should be given to patients with severe Covid-19 symptoms, for two reasons.
Harvard University investigators recommend their use because they have anti-inflammatory powers.
Scientists added last month in the journal Drug Development and Research that statins have also shown an ability to moderate the immune system and thus protect patients’ lungs from cytokine storm damage.
Professor Jon Cohen, emeritus professor of infectious diseases at Brighton and Sussex Medical School, argues that while statins have shown potential in test-tube trials, in living patients they have only really shown benefits for the cardiovascular system.
In normal circumstances viruses develop a ‘key’ that enables them to pick a cell’s locks and break in, hijacking the cell’s machinery to make more copies of the virus. Peptide inhibitors stick to this key, rendering it unable to do its job.
We already know that Covid-19 invades human cells through a protein receptor, ACE2.
The big question, therefore, is: what might block the coronavirus attaching to the ACE2 receptor?
Chemists at Illinois University used high-powered computers to identify the amino-acid chemicals in the ACE2 receptor that the virus targets. They then constructed a drug with amino-acids that should stick to the virus’s key, rendering it useless.
But as the scientists acknowledge in journal ACS Nano this month, they have tested their chemical in computer simulations — not in the lab and certainly not on humans. A lot of hurdles lie ahead.
Ultimately, most scientists agree that coronavirus prevention — a vaccine — is better than any treatment or cure.
That’s why governments are throwing the proverbial kitchen sink at efforts to create one, with more than 140 projects currently running in parallel all over the world.
Everyone expects a vaccine to appear in the end. But much hinges on how quickly that happens.
That’s why there was so much excitement this week when it emerged that scientists at Oxford University have already begun to conduct their first human vaccine tests.
Other clinical trials in humans are already underway in China.
Nevertheless, Professor Chris Whitty, England’s Chief Medical Officer, says the chance of a vaccine becoming available in the next calendar year are ‘incredibly small’.
Why? Because we can move only as quickly as extreme caution will allow, says inoculation expert Dr Kai Hu of Imperial College. He reports Imperial’s lab has already created a harmless ‘pseudo-virus’ that carries a coronavirus protein. But, he stresses: ‘Safety is our number one priority. We don’t yet know how toxic the vaccine would be to humans.’
Given Covid-19’s devastating infectiousness, the world will have to keep its fingers crossed that the dash for an effective jab proves a success — rather than inadvertently plunging humanity into further peril.
Three members of the same family are taking part in a groundbreaking coronavirus vaccine trial. Mum Katie, dad Tony and daughter Rhiannon Vinney are among more than 1,000 participants taking part in the Oxford University trials.
Teaching assistant Katie, 46, saw the plea for healthy volunteers and urged her husband, 53, who runs two pubs, and their 18-year-old student daughter to sign up with her.
The mum-of-four, from Oxford, said she was not worried about health risks from taking part, because she believes the team have done everything they could to make it safe.
She added: ‘I just want to help so life can return to normal. You have to live in a cave not to know somebody who is affected by this. I really do hope this is the cure.’