Life before a vaccine: How can Covid be treated and could we become immune?
Video report by ITV News Science Editor Tom Clarke
Words by ITV News Multimedia Producer Narbeh Minassian
The race to develop a vaccine for Covid-19 is well underway and could be ready at the start of next year.
A process that usually lasts years has been sped up at such a rate that there are more than 40 vaccines in human trials worldwide, with almost 200 in pre-clinical stages.
A vaccine with proven success will protect the public from infection in the first place - but until then, treatments are needed to mitigate the virus’ effects and, ultimately, cure patients.
There have been more than 50 million cases globally - more than 1,000,000 of which are in the UK – and doctors are looking at signs of immunity in those who have recovered.
The good news is that treatments are expected much sooner than a vaccine as scientists are exploring the potential to repurpose drugs already known to be safe.
The better news is many of us may already have some kind of immunity to the virus already.
So which drugs and treatments have shown promise? And could we develop a natural immunity?
The work going into treatments
The UK is running the world’s largest clinical trial right now, with more than 11,500 patients at 176 NHS hospitals.
The Recovery trial, as it has been dubbed, is testing a range of existing medicines including drugs for treating HIV to see if they have a benefit for Covid-19 patients.
It stopped giving patients the anti-malaria medicine hydroxychloroquine, for example, after it was found to show no benefit.
Another arm of the Recovery trial is giving patients plasma taken from the blood of those who have recovered from Covid-19.
Another trial in the UK could see volunteers who have had a vaccine candidate deliberately exposed to the virus in order to speed up trials.
The World Health Organization (WHO) kickstarted the Solidarity Trial, so far recruiting 5,500 patients from 39 countries.
More than 100 countries have either joined or expressed an interest in the trial.
The WHO supports all participants by shipping requested drugs, training clinicians and identifying hospitals taking part.
What do these treatments need to do to be effective?
To understand how and why drugs already on the market can be effective, let’s first look at how exactly Covid-19 causes illness, both directly and indirectly.
The first answer is that that virus itself causes health complications – in Covid-19’s case it attacks the lungs and can leave patients finding it difficult to breathe.
So the obvious response to this is to find an anti-viral drug that can directly combat the coronavirus cells – which is something the much-talked-about remdesivir does.
But major problems can also be induced and exacerbated by an overreaction from our immune system.
This means treatments need to either target the virus itself or inhibit excessive reactions from the immune system. What effective drugs have been identified?
Drugs are not the only way to potentially treat the virus but a major breakthrough has been made already.
Perhaps the most significant find so far is Dexamethasone - an anti-inflammatory drug used to treat arthritis.
A UK trial in June proved Dexamethasone can save one life for every eight patients on ventilators in the UK.
For people needing oxygen, the drug also helps cut the death rate by 20%.
Dexamethasone has been tested as part of the Recovery trial and scientists say 4,000 to 5,000 deaths could have been prevented in the UK alone, had they known about the drug’s effectiveness earlier.
Dr Masahiro Ono, an immunologist at Imperial College London, explains how the immune system’s overreaction – which dexamethasone limits - can lead to the most severe cases.
“In order to prevent immune cells from over-reacting and damaging the lung and other tissues, dexamethasone has been shown effective and in use in clinical practice,” he told ITV News.
“It is thought that people develop severe disease by their excessive immune responses to the virus, which can increase the damage to the lungs.
“This leads to pneumonia and respiratory distress.
“In addition, the overreaction of immune cells, such as T-cells, can further activate other immune cells, leading to a more complicated disease condition known as Cytokine Storm.
“This can result in circulation problems, infarction of organs and death. However, we still do not know what factors determine the vulnerability to such overreactions.”
Dexamethasone is the only drug so far that has been proven to save lives but there is hope for anti-viral drug remdesivir, which was used against Ebola.
The WHO has it listed as a treatment under study and early results of the international trial have revealed that remdesivir is a potential breakthrough.
It has been approved for use in Covid-19 patients by the US and the UK, among other countries, after data suggested it can cut recovery time by about four days.
However, there is no clinical trial data as yet to suggest it improves survival from coronavirus.
On the drug’s effectiveness, The WHO said: “It has generated promising results in animal studies for Middle East Respiratory Syndrome (MERS-CoV) and severe acute respiratory syndrome (SARS), which are also caused by coronaviruses, suggesting it may have some effect in patients with Covid-19.”
Is there another treatment available?
The UK began trialling a possible treatment using the plasma from recovered Covid-19 patients in early May.
It is hoped the potential treatment, known as convalescent plasma, will help patients whose bodies are not producing enough antibodies to fight the disease.
“Convalescent patients have developed antibodies against coronavirus, which can help other people to fight coronavirus,” Dr Ono said.
“Some antibodies in each of those patients can block infection - such antibodies are called neutralising antibodies - and we expect that convalescent blood plasma contains such antibodies and could protect vulnerable people from infection when the plasma is transferred into them.”
Another new drug which has hit the headlines recently is REGN-COV2, developed by Regeneron Pharmaceuticals. Despite being in the early stages of testing and yet to be fully approved by the medical industry, the drug was given to President Donald Trump after his positive Covid diagnosis.
REGN-COV2 is made up of two monoclonal antibodies (REGN10933 and REGN10987), which are man-made to act like human antibodies in the immune system.
It was first tested on mice which were genetically modified to have a human immune system, before being tested on 275 people, of whom 40% were classed as obese.
The antibody cocktail works by binding to a protein on the surface of the virus, stopping it from attaching to cells and replicating, while allowing the immune system to attack the virus.
Regeneron has linked up with the pharmaceutical giant Roche to increase the global supply of REGN-COV2 if it proves effective.
Professor Peter Hornby, who specialises in emerging medicines for infectious disease, said early trials have been "very promising".
He said: “In the laboratory, in cell cultures, it has a very strong effect against the virus, and there have been studies in artificial animals where it also shows benefits.
“So probably of the drugs that are available, it’s one of the most promising.”
What about Hydroxychloriquine?
Used against malaria, Hydroxychloriquine had been heralded by some as a potential treatment – even by President Donald Trump and his Brazilian counterpart Jair Bolsonaro.
But both the UK Recovery trial and the WHO’s Solidarity trial have halted all investigations into its use against coronavirus after concluding it does not save lives.
How does our immune system work?
There are essentially two lines of defence – the innate and the adaptive immune systems.
The former organises the initial response to foreign pathogens inside the body, while the latter tailors a specific defence to that particular bug.
It’s within these specially-made responses where antibodies and T-cells play a key role.
Antibodies, produced by B-cells from the bone marrow, are made for specific cells – which is why those who recover are likely to have Covid-19 antibodies.
They lock on to the invading cell and mark it for destruction by other immune cells, which is when T-cells come in to play.
Dr Ono is an expert on T-cells investigating how they control immune reactions and how they can overreact to Covid-19.
“T-cells are fascinating as they can memorise what infection they encounter within the past and make specific and effective responses to the same infections,” he said.
“This way, some T-cells coordinate other immune cells to optimise specific immune response to each infection, while other T-cells can directly recognise and remove virus-infected cells.”
Could we become immune?
It is possible that those infected could become immune to some extent to the virus, though how long that could last is not yet known for sure.
According to a study in October, which showed a decline in protective antibodies, immunity could only last a few months following infection.
Research by Imperial College London estimated just 4.4% of adults had some form of immunity against Covid-19 in September, when cases began to increase again. This is compared with 6% found to have antibodies between June 20 and July 13, and 4.8% between July 31 and August 31. Findings published by Imperial College London and Ipsos MORI suggest that people who did not show symptoms of the virus were likely to lose antibodies sooner than those who did show symptoms. Those aged 18-24 had the highest prevalence of antibodies and lowest decline in antibody levels at 14.9%. Meanwhile, people aged 75 and over had the lowest prevalence and saw the largest drop, with antibody levels falling by 39%. Researchers warned, however, that it remains unclear whether antibodies provide any effective level of immunity or, if such immunity exists, for how long it might last.
Surveying more than 365,000 participants across England, researchers found the number of people with antibodies to coronavirus fell by 26.5% over three months.
Perhaps a more encouraging possibility is that many of us may already have some kind of immunity before ever contracting Covid-19.
International science journal Nature Research published a review on pre-existing to Covid-19 and made some interesting conclusions.
“It is now established that SARS-CoV-2 (Covid-19) pre-existing immune reactivity exists to some degree in the general population,” it stated.
“It is hypothesized, but not yet proven, that this might be due to immunity to CCCs (‘common cold’ coronaviruses).
“This might have implications for Covid-19 disease severity, herd immunity and vaccine development, which still await to be addressed with actual data.”
Measuring T-cells could be better at tracking spread of Covid-19 than antibodies
Coronavirus immunity may only last a few months, study suggests
In other words, T-cells derived from exposure to other viruses from the coronavirus family may have the ability to put up a defence against Covid-19, at least to some extent.
Dr Ono explains researchers are investigating how much immunity is established and how long it is maintained.
“Recent studies using antibody testing have shown that antibodies against coronavirus tend to decay quite quickly – within several months,” he said.
“On the other hand, other studies have shown that, in addition to antibodies, coronavirus-specific T-cells are successfully induced in convalescent patients.
“This means that some T-cells are capable of remembering the virus and are ready to fight against them.
“We still do not know how much and how long such coronavirus-specific T-cells can be maintained and provide immunity against coronavirus.”
Could the virus mutate?
“Any such viruses are all mutated at some rate – which is not surprising and not worrying by itself,” said Dr Ono.
“The question is, if there is any risk that the virus is mutated enough to acquire new abilities - for example, to become more infectious.
“To date, there is no such evidence - and most researchers think that there is still only one virus – SARS-CoV-2 - which can induce various symptoms because different people’s immune systems may react differently to the virus.”