Coronavirus: five months on, what scientists now know about Covid-19
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Coronavirus: five months on, what scientists now know about COVID-19 |
Medical researchers have been studying everything we know about coronavirus. What have they learned – and is it enough to halt the pandemic?
Coronaviruses have been causing problems for humanity for a
long time. Several versions are known to trigger common colds and more recently
two types have set off outbreaks of deadly illnesses: severe acute respiratory
syndrome (Sars) and the Middle East respiratory syndrome (Mers).
But their impact has been mild compared with the global
havoc unleashed by the coronavirus that is causing the COVID-19 pandemic. In
only a few months it has triggered lockdowns in dozens of nations and
claimed more
than 145,000 lives. And the disease continues to spread.
That is an extraordinary achievement for a spiky ball of
genetic material coated in fatty chemicals called lipids, and which measures 80
billionths of a meter in diameter. Humanity has been brought low by a very
humble assailant.
On the other hand, our knowledge about the Sars-CoV-2, the
virus that causes COVID-19, is also remarkable. This was an organism unknown to
science five months ago. Today it is the subject of study on an unprecedented
scale. Vaccines
projects proliferate, antiviral drug trials have been launched and new
diagnostic tests are appearing.
The questions are therefore straightforward: what have we learned over the past five months and how might that knowledge put an end to this pandemic?
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Coronavirus: five months on, what scientists now know about COVID-19 |
Where did it come from and how did it first infect humans?
The Sars-CoV-2 virus almost certainly originated
in bats, which have evolved fierce immune responses to viruses,
researchers have discovered. These defenses drive viruses to replicate faster
so that they can get past bats’ immune defenses. In turn, that transforms the
bat into a reservoir of rapidly reproducing and highly transmissible viruses.
Then when these bat viruses move into other mammals, creatures that lack a
fast-response immune system, the viruses quickly spread into their new hosts.
Most evidence suggests that Sars-CoV-2 started infecting humans via an
intermediary species, such as pangolins.
Coronavirus statistics: what can we trust and what should we ignore?
“This virus probably jumped from a bat into another animal,
and that other animal was probably near a human, maybe in a market,” says
virologist Professor Edward Holmes of Sydney University. “And so if that
wildlife animal has a virus it’s picked up from a bat and we’re interacting
with it, there’s a good chance that the virus will then spread to the person
handling the animal. Then that person will go home and spread it to someone
else and we have an outbreak.”
As to the transmission of Sars-CoV-2, that occurs when
droplets of water containing the virus are expelled by an infected person in a
cough or sneeze.
How does the virus spread and how does it affect people?
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Virus-ridden particles are inhaled by others and come into
contact with cells lining the throat and larynx. These cells have large numbers
of receptors – known as Ace-2 receptors – on their surfaces. (Cell receptors
play a key role in passing chemicals into cells and in triggering signals
between cells.) “This virus has a surface protein that is primed to lock on
that receptor and slip its RNA into the cell,” says virologist Professor
Jonathan Ball of Nottingham University.
Once inside, that RNA inserts itself into the cell’s own
replication machinery and makes multiple copies of the virus. These burst out
of the cell, and the infection spreads. Antibodies generated by the body’s
immune system eventually target the virus and in most cases halt its progress.
“A COVID-19 infection is generally mild, and that really is
the secret of the virus’s success,” adds Ball. “Many people don’t even notice
they have got an infection and so go around their work, homes, and supermarkets
infecting others.”
By contrast, Sars – which is also caused by a coronavirus –
makes patients much sicker and kills about one in 10 of those infected. In most
cases, these patients are hospitalized and that stops them from infecting others –
by cutting the transmission chain. Milder COVID-19 avoids that issue.
Why does the virus sometimes cause death?
Occasionally, however, the virus can cause severe problems.
This happens when it moves down the respiratory tract and infects the lungs,
which are even richer in cells with Ace-2 receptors. Many of these cells are
destroyed, and lungs become congested with bits of the broken cells. In these cases,
patients will require treatment in intensive care.
Even worse, in some cases, a person’s immune system goes
into overdrive, attracting cells to the lungs in order to attack the virus,
resulting in inflammation. This process can run out of control, more immune
cells pour in, and the inflammation gets worse. This is known as a cytokine storm. (In
Greek, “cyto” means cell and “kino” means movement.) In some cases, this can
kill the patient.
Just why cytokine storms occur in some patients but not in
the vast majority is unclear. One possibility is that some people have versions
of Ace-2 receptors that are slightly more vulnerable to attacks from the
coronavirus than are those of most people.
Are we protected for life if we arrange infected?
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Coronavirus: five months on, what scientists now know about COVID-19 |
Doctors examining patients recovering from a COVID-19 infection are finding fairly high levels of neutralizing antibodies in their blood. These antibodies are made by the immune system, and they coat an invading virus at specific points, blocking its ability to break into cells.
“It is clear that immune responses are being mounted against
COVID-19 in infected people,” says virologist Mike Skinner of Imperial College
London. “And the antibodies created by that response will provide protection
against future infections – but we should note that it is unlikely this
protection will be for life.”
Instead, most virologists believe that immunity against
COVID-19 will last only a year or two. “That is in line with other
coronaviruses that infect humans,” says Skinner. “That means that even if most
people do eventually become exposed to the virus, it is still likely to become
endemic – which means we would see seasonal peaks of infection of this disease.
We will have reached a steady-state with regard to COVID-19.”
The virus will be with us for some time, in short. But could
it change its virulence? Some researchers have suggested that it could become
less deadly. Others have argued that it could mutate to become more lethal.
Skinner is doubtful. “We have got to consider this pandemic from the virus’s
position,” he says. “It is spreading around the world very nicely. It is doing
OK. Change brings it no benefit.”
In the end, it will be the development and roll-out of an
effective vaccine that will free us from the threat of COVID-19, Skinner says.
When will we get a vaccine?
Last Friday, the journal Nature reported that
78 vaccine projects had been launched around the globe – with a further
37 in development. Among the projects that are underway is a vaccine program
that is now in phase-one trials at Oxford University, two others at US
biotechnology corporations and three more at Chinese scientific groups. Many
other vaccine developers say they plan to start human testing this year.
This remarkable response raises hopes
that a COVID-19 vaccine could be developed in a fairly short time.
However, vaccines require large-scale safety and efficacy studies. Thousands of
people would receive either the vaccine itself or a placebo to determine if the
former were effective at preventing infection from the virus which they would
have encountered naturally. That, inevitably, is a lengthy process.
As a result, some scientists have proposed a way to speed up
the process – by deliberately exposing volunteers to the virus to determine a
vaccine’s efficacy. “This approach is not without risks but has the potential
to expedite candidate vaccine testing by many months,” says Nir Eyal, a
professor of bioethics at Rutgers University.
Volunteers would have to be young and healthy, he stresses:
“Their health would also be closely monitored, and they would have access to
intensive care and any available medicines.” The result could be a vaccine that
would save millions of lives by being ready for use in a much shorter time than
one that went through standard phase three trials.
But deliberately infecting people – in particular, volunteers
who would be given a placebo vaccine as part of the trial – is controversial.
“This will have to be thought through very carefully,” says Professor Adam Finn
of Bristol University. “Young people might jump at the opportunity to join such
a trial but this is a virus that does kill the odd young person. We don’t know
why yet. However, phase-three trials are still some way off, so we have time to
consider the idea carefully.”
• This article was amended on 12 April 2020. The
original version incorrectly described the COVID-19 virus as measuring “an
80-billionth of a meter”, when it should have said “80 billionths of a meter”.
A quote from Mike Skinner, responding to whether COVID-19’s virulence could
change, was also corrected.
Due to the unprecedented and ongoing nature of the
coronavirus outbreak, this article is being regularly updated to ensure that it
reflects the current situation as best as possible. Any significant corrections
made to this or previous versions of the article will continue to be footnoted
inline with Guardian editorial policy.
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