Scientists race to answer six key questions about the coronavirus

Since a novel pneumonia was discovered in Wuhan in central China scientists around the world have been working at breakneck speed to understand this new disease.

They have sequenced the genome, started developing a vaccine and begun trialling treatments. But despite these advances, there is still a lot we don't know.

Click a question below to reveal how experts are tackling these unknowns - and how close we are to solving them.

This is the million dollar question and has been the subject of intense speculation and debate. While the virus is thought to have emerged in a live animal market in Wuhan scientists are still unsure of the original animal host.

Some conspiracy theorists have said that the virus was engineered in a lab in China and some have even pointed to a link between it and 5G phone technology - and have even burned down mobile phone masts.

The US government has also highlighted the fact that because the Wuhan Institute of Virology - where coronaviruses have been intensively studied - is based in the city where the disease emerged the pandemic may have escaped from one of its labs, either by accident or design.

While this is theoretically possible most experts say that the disease has evolved naturally and it most likely came from bats, the source of many zoonotic diseases such as Ebola.

Some of the firmest evidence yet comes from a study in May which looked at 227 samples taken from bats in caves in Yunnan province. They identified a virus – called RmYN02 – which closely resembles SARS-CoV-2, the virus that causes Covid-19.

One reason behind the speculation that Covid-19 was manipulated in the laboratory is because of an unusual mutation in the virus’s protein. The Chinese scientists found that this same mutation occurs in the recently discovered bat coronavirus. This gene shares 93 per cent of its genetic material with Sars-Cov-2, the virus that causes Covid-19.

However, according to an article in the journal Nature scientists would need to find an animal that hosts a version more than 99 per cent similar to SARS-CoV-2 — a prospect complicated by the fact that the virus has spread so widely among people, who have also passed it to other animals, such as cats, dogs and farmed mink.

Since the virus first emerged in January around 170 vaccine candidates are now in development, with 15 already in human trials - this is science moving at unprecedented speed. Compare that to Aids which emerged in the 1980 and for which there is still no viable vaccine.

One of the front runners in the coronavirus race is being developed by Oxford University and Astra Zeneca, which will soon move into phase III trials in Brazil. Another candidate being developed by US firm Moderna is hot on its heels.

However, a vaccine is not a given, says Dr Seth Berkley, chief executive of Gavi, the Vaccine Alliance.

“Vaccine candidates have a normal success rate of around seven per cent preclinical, maybe 15 to 20 per cent clinical so the vast majority will fail. But by having a large portfolio this will move us forward,” he says.

And while the Oxford candidate may be first out of the traps animal studies showed that it did not stop monkeys getting the disease but it did reduce disease severity.

Dr Nick Jackson, head of programmes and technology at Cepi, which provides funding for vaccine development, said the first vaccine is unlikely to be the best.

"There are a number of examples historically where the first vaccine is far from superior and it is the second generation vaccine that works better. The first vaccine may not be the best but it will be suitable for dealing with the pandemic," he said.

Covid-19 affects people in wildly different ways. It is estimated that around 40 per cent of infections are asymptomatic or are so mild they’re barely noticeable. While other sufferers, including those who don’t end up in hospital, are wiped out for weeks and report a range of long-term complications such as breathlessness and fatigue.

While older people and those with underlying conditions, particularly diabetes, are more at risk of the more severe forms of the disease, scientists are still unsure why Covid-19 affects people in such wildly differing ways.

However, new evidence is emerging that genetics may play a part. German researchers found two points in the human genome which were associated with an increased risk of respiratory failure in patients with Covid-19. One of these points is the gene that determines blood type.

Patients with blood type A were 50 per cent more likely to need oxygen or go on a ventilator, the researchers found.

However, Andre Franke, professor of molecular medicine at the University of Kiel and lead author of the study, said it was not certain whether it was the blood group that determined whether someone would become more seriously ill, or the genetic marker.

“We cannot disentangle yet whether actually the blood group is the risk or some genetic variants that are linked to the blood groups,” said Prof Franke.

A team at Rockefeller University in New York is  now looking at the genomes of healthy younger people who have experienced the more severe cases of Covid-19.  Extreme susceptibility to other infections, including tuberculosis and Epstein–Barr virus have been linked to mutations in single genes and experts believe the same will be true of this coronavirus.

Knowing how long immunity lasts is crucial for the development of a vaccine and for identifying who should get it first. However, recent studies have shown that immunity may quickly wane.

One study found that 10 per cent of patients hospitalised with Covid-19 in China had undetectable antibodies just weeks after recovering from the disease.

The other antibody study, published in the journal Nature Medicine, compared two groups of people who contracted the disease in Wanzhou, China in February. They looked at 37 people who had asymptomatic cases of the disease and 37 who had more severe forms.

They found that 40 per cent of people in the asymptomatic group had undetectable levels of antibodies two to three months after the infection, compared to 13 per cent in the group who had a more severe dose of the disease.

Antibody testing has been highlighted as a route out of the pandemic with so-called “immunity passports” being issued to people who have good antibody responses. However, these studies show the limits of such tests.

Another recent study showed that researchers may be looking in the wrong place and that it is T-cells, not antibodies, that are crucial in the fight against the disease. This research, showed that 81 per cent of the 185 people they tested who had not had the disease had a T-cell response to Sars-Cov-2, the virus that causes Covid-19. And this immune response was linked to previous exposure to common cold coronaviruses, the researchers found.

This is not the first study to link exposure to the common cold to immunity to Covid-19 and some believe that one reason children and younger people are less susceptible to the disease is because they are regularly exposed to coughs and sneezes.

Since the outbreak first emerged in January various studies have pointed to mutations in Sars-CoV-2, the virus that causes Covid-19. But virologists point out that viruses mutate all the time and it will only be if we see a dramatic change in death rates or the number of infections that we will understand if there has been a mutation.

Last week Dr Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases in the US and leader of the government’s coronavirus taskforce, said there is data to suggest the existence of a new mutation of Covid-19 which is more “transmissible”.

He cautioned that scientists are still trying to confirm its existence and it does not appear to be more damaging for people who catch that strain of the virus.

Coronaviruses don’t like the heat or sunlight and there has been some speculation that the virus will come back with a vengeance during the winter months.

The Spanish flu pandemic of 1918 to 1920 went around the world in waves, peaking during the coldest times of the year.

But when asked whether the recent spike in cases seen in Melbourne is linked to the Australian winter, Keith Neal, emeritus professor of the epidemiology of infectious diseases at the University of Nottingham, said it is too early to say whether Covid-19 will resurge when the weather turns colder.

“The virus does not like heat and some aspects of humidity. How much this actually helps we do not know. The USA and India are going into their summer and seeing cases rise.

“It is far too early to draw any conclusions about how going into winter will affect this virus.  Winter in parts of Australia is very different from our winters," he said.

In the UK, the main risk in winter may be that we're huddled indoors in poorly ventilated rooms, he added.

“We know that outside transmission risks are very low especially if social distancing is maintained,” he said.

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