IT is now seven months since the World Health Organisation first became aware of a “viral pneumonia of an unknown cause” among a cluster of patients in Wuhan, China.

So after 17 million cases of Covid-19 worldwide and at least 668,000 deaths, how far have we come in unlocking the disease?

The first study into the prevalence of Covid-19 antibodies in Scotland using blood samples from 4,751 people suggests that around 4.8 per cent of the population has been exposed so far.

If so, that would mean that a virus which had infected 261,792 Scots by June 20 - when the pilot ended - has a mortality rate of between 0.9% and 1.6%, depending how you count Covid deaths.

So is it really the case that more than 95% of the population is still susceptible?

“I think that’s probably an underestimate,” says Professor Eleanor Riley, an expert in immunology and infection research at Edinburgh University, when asked about the 4.8% figure.

“We know that people who’ve had asymptomatic infections make very few antibodies, so they may turn out negative, whereas people who were quite severely ill seem to make a lot of antibodies which last for quite a long time.

“The true prevalence is likely higher, but I don’t know how much higher.”

Antibodies are proteins generated by the immune system to seek out and destroy pathogens circulating in our bodies.

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Because they are created even when people experience only mild - or even no - signs of illness, they can be used to track how extensively a disease is spreading in a population, beyond the numbers thrown up by hospital admissions or people sick enough to seek out a test.

Recent research from a Spanish antibody study - the largest to date - suggests that somewhere between 22% and 36% of those infected with the virus develop no symptoms.

Covid antibodies also seem to fade quickly, sometimes to undetectable levels.

A study of more than 90 patients and healthcare workers at King’s College London was the first to monitor antibodies over three months from the onset of symptoms.

It found that only 17% still had “potent” levels of these proteins by the end of the study period, leading to comparisons with the fragile immunity seen in coronaviruses responsible for the common cold.

“One thing we know about these coronaviruses is that people can get reinfected fairly often,” said Prof Stuart Neil, a co-author on the study.

“What that must mean is that the protective immunity people generate doesn’t last very long.

“It looks like Sars-Cov-2, the virus that causes Covid-19, might be falling into that pattern as well.”

This might sound worrying, but there are two important caveats.

Firstly, it is actually completely normal for antibodies to decline over time.

Secondly, they are not the only immune cells which fight infection.

Antibodies are designed to eliminate the virus from bodily fluids like blood, thus preventing infection.

But once a virus gets inside cells, it is up to ‘killer T’ white blood cells to attack.

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Furthermore, the immune system can also manufacture something called memory B cells, which are stored away in the spleen or lymph glands with a sort of antibody ‘recipe card’ ready to regenerate them should a particular infection strike again.

Evidence is already emerging for both in relation to Covid-19.

“There are one or two papers showing that people who have been infected do generate these memory responses, so the expectation is that those will quickly regenerate antibodies if people get infected a second time,” said Prof Riley.

“There are also papers starting to come out looking at the T cell responses in patients - in people with severe disease, and those with less severe disease.

"And in fact, the T cell response seems to be strong in people who’ve had mild disease as well as severe disease.

“We can also find T cells in people where there was no evidence of them ever having had the disease. So it seems the T cell response is rather more universal than the antibody response.”

Researchers in Germany also found that one in three people with no prior exposure to Sars-Cov-2 have T cells capable of recognising the virus, possibly due to prior infection with a common cold virus.

This type of cross-reaction is not unusual in the immune system, and might explain the comparatively high rates of mild to asymptomatic infection.

But work is ongoing to determine whether they actually provide any protection against Covid-19.

Professor Dr Leif Erik Sander , one of the researchers at Universitätsmedizin Berlin, said: “It is possible that cross-reactive T-helper cells have a protective effect, for instance by helping the immune system speed up its production of antibodies against the novel virus.

“In this case, a recent bout of the common cold would probably result in less severe Covid-19 symptoms.

“However, it is also possible that cross-reactive immunity could lead to a misdirected immune response and potentially negative effects on the clinical course of Covid-19.

"We know this can occur with dengue fever, for instance.”

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Either way, a vaccine which mimics the immune system response to severe infection remains the most hopeful route out of this pandemic.

There are already 250 candidate vaccines worldwide, with around 20 in active clinical trials.

Preliminary results from the UK vaccine trial led by Oxford University found that theirs induces strong T cell and antibody responses within weeks, although it is unclear how long this lasts or if it actually prevents infection.

Kate Bingham, chair of the UK vaccine taskforce said last week she expects that an eventual Covid-19 vaccine will only mitigate disease or require annual boosters, as opposed to providing the lifetime immunity of a measles innoculation, for example.

Prof Riley says it is too early to speculate, adding that - ironically - the low prevalence of the virus in the UK now is one of the few things slowing progress.

"I don't think we could hope to be in a better place as far as vaccines go than we are at this stage," she said.

“Everything is going as fast as it can. The only thing that would speed it up now [in terms of testing the effectiveness of the vaccine] would be if there was a second massive wave of infection in the UK and all of those vaccinated and in control groups got it, which is the last thing we actually want to happen.

"We can’t have it all: we can’t have an absolute answer to the vaccine question and keep cases down. They are testing the vaccine in South Africa and Brazil where the virus is not under control. It may well be observation from there that gets us the efficacy data.”