The coronavirus has now been with us for over a year.
During that time, our knowledge about the virus
and the disease it causes has increased dramatically.
MATT HANCOCK: We have identified a new variant of coronavirus
which may be associated with the faster spread
in the southeast of England.
In this Horizon special, we will be bringing you up to speed
on what we know now.
Providing you with answers direct from the army of scientists
and clinicians on the front line of the fight against Covid-19.
You didn't need a sample of virus?
No, we absolutely didn't.
We just needed to know the coding sequence.
We'll be telling you the latest information
about how and why viruses mutate...
Well, we were so shocked.
We'd all been told for many months that this was a virus
that doesn't really mutate very fast.
..how the new vaccines work and how they were created so quickly...
We can very quickly adapt the sequence in the vaccine
to adapt to those new variants.
..and how identifying coronavirus super-spreaders
can help reduce infection rates.
In the two weeks after one of these initial cases appears,
you can potentially double the number
of onward transmission events that you prevent.
And with the announcements this week laying out a road map
to lifting restrictions,
we'll also be tackling the biggest question of all -
when can we get back to normal?
Everything we're now experiencing
is because of this tiny pathogen's
overriding evolutionary purpose -
to reproduce.
Like all viruses, it acts as a parasite.
It can only reproduce by infecting us
and hijacking our own cells' reproductive machinery.
But incredible developments in genetics
and genetic engineering mean that we are fighting back
in ways we simply couldn't have, even five years ago.
The coronavirus has also moved on, though.
It's changing shape, it's becoming harder to pin down.
So far, we've seen new variants emerge around the globe -
South Africa, Brazil and, of course, much closer to home.
In November last year,
thanks to a strict national lockdown,
Covid cases in the UK fell for the first time in months.
But in Kent, it was a different story.
There, infections were rising dramatically.
NEWSREADER: Swale in Kent is now the second-worst hit
area in the country.
NEWSREADER: High numbers in a couple of areas of Kent
have pushed the whole county into the toughest restrictions.
Something didn't add up,
so geneticists set about decoding the genome
from this worrying new surge in the Garden of England.
What they discovered was a new variant
with dangerous mutations.
At the beginning of the pandemic,
an organisation called COG-UK was set up
to keep tabs on how the virus might evolve.
They've been doing that by decoding the genomes
of hundreds of thousands of positive Covid samples.
Positive tests taken outside of hospital come here,
to the Wellcome Sanger Institute in Cambridge.
It's a huge operation.
Over 300 people work here.
Dr Ewan Harrison showed me around.
These, they're a mix of positive and negative samples.
And then the robotics you see here pick out the positives.
OK.
These machines decode the genetic material
and upload it to a database.
Then, by comparing the new samples with the original strain,
scientists can spot mutations.
Why are you particularly interested in the information about mutations?
We expect to see about one to two mutations a month,
accruing in a particular virus as it transmits between people.
And mutations, in many ways, act like a barcode.
So they allow us to tell the difference between
two types of the virus.
So, if two people have types of the virus
that have different mutations,
then we know that likely they got the virus
from two different sources,
and that's the fundamental basis of why we're doing the sequencing.
It allows us to tell whether two viruses
are related to each other or are different.
When any organism - including a virus - reproduces,
mutations are created in its genome.
If those mutations confer an evolutionary advantage,
they will be passed on to future generations.
To begin with, this virus accumulated just one or two
mutations each month.
But that suddenly changed at the end of 2020.
But what we saw in the particular cluster of cases
that were in the southeast of England
is that they had 23 different mutations across the virus.
It suddenly jumped to having 23?
Yeah. I mean, it was a surprise.
MATT HANCOCK: We have identified a new variant of coronavirus
which may be associated with the faster spread
in the southeast of England.
The new variant of coronavirus has a much quicker transmission rate
than the original strain.
The new variant of coronavirus is spreading rapidly.
The new variant... The new variant...
The new variant of coronavirus is out of control.
The new mutation was spreading at an alarming rate.
Professor Ravi Gupta was determined to find out why.
What went through your head when you realised there was a new variant,
there was something spreading fast and it had 23 mutations
coming out of the southeast of England - the new variant?
Well, we were so shocked
that we almost didn't believe the sequencing, you know?
We'd all been told for many months that this was a virus
that doesn't really mutate very fast.
Ravi works as a clinician at Addenbrooke's Hospital.
There, he saw a patient whose immune system had been weakened
by chemotherapy, and who'd been sick with Covid-19
for over three months.
That case would reveal a vital clue about how the virus could evolve
so quickly in other parts of the country.
So, he'd been infected for 100 days,
and part of the reason was the fact that his immune system
wasn't working properly.
And that allowed the virus to keep replicating
and making a lot of copies.
Doctors administered antibodies donated from recovered patients,
hoping they would help fight the virus.
Unfortunately, there was so much virus there
that the antibodies couldn't cure the patient of a Covid-19.
But what it did allow is for that virus to learn
how to get around those antibodies.
We noticed that the virus started shifting,
it started making mutations.
By the time the patient died,
Ravi's team had identified 37 mutations in the virus.
This led scientists to believe that new variants
like the one found in Kent
may evolve in the bodies of patients with weakened immune systems.
Most of us, of course, clear this virus in a week or so.
This patient had it for many, many weeks.
And because they were being exposed to new antibodies,
that is what gave that virus an accelerated chance to evolve?
That's right. And so we were fairly certain that this is the cause
for the new variants that are circulating around the world
at the moment.
Mutations in the spike protein may also affect
how our current vaccines work.
The spike is the part of the virus that they target.
We're now in the era of vaccination,
but there will be more pressure on this virus
to adopt mutations that enable it to avoid
vaccinated people's immunity.
And I can already see there are three or four mutations
causing us severe trouble.
So we already need to change our vaccines in the immediate future,
and we'll probably need to do it in the years to come.
Mutations are a huge concern.
As long as there is transmission, this virus will continue to evolve.
Now, the variants we've seen so far don't appear
to be much more deadly. Our vaccines do still work.
But variants will emerge that can escape the vaccine,
and when they do, it's the people here and at Wellcome Sanger
that are going to be the first to know.
I'm joined by Professor Sharon Peacock.
She's the director of Covid-19 at Genomics UK,
also known as COG-UK,
a consortium set up to monitor the progress of the virus
and also advise the UK Government.
Sharon, by now everyone has heard of at least four variants -
South Africa, Brazil, the UK, and now Nigeria.
What are the things that we worry about
with each of these variants?
The first is, is a virus more transmissible?
The second is, will it avoid our immune system?
The third is, could it be more lethal for us
and kill more people?
And finally, could it affect our diagnostic tests and avoid them?
We've got a graphic here of UK variants.
So, if we look at the cluster of red bars, there,
what we're seeing there is a variant that first arose probably in Spain,
and it appeared to transmit very rapidly
and markedly throughout Europe.
And that is summer holiday travel.
And so this particular variant was transmitted by people
travelling during their summer holidays
and importing this, and it moving around Europe through travel.
And it's a large number of people carrying this virus back
that account for the large number of cases -
it's NOT that it's good at spreading.
Now, with the sort of greeny-yellow one
that then really explodes from sort of mid-December
out to the current time.
So that's the variant that we've all become very familiar with now -
B117, or some people refer to it as the Kent variant.
And so, if you look at the green,
by the time you get to around mid-November,
that you start to see cases beginning to increase,
and is now by far and away the most common cause
of Covid-19 in this country.
Now, the difference there is it WAS the virus
that had changed its biology
and had led to more rapid transmission between people.
So it spread through the population very quickly -
not a function of people transmitting it
through travel or similar,
but because of a property of the virus.
So a variant might be fitter if it's more able to transmit.
What about changes that we see in these variants
that allow them to evade the immune system?
We know about the, quite famous now, mutation E484K.
That's a very good example of where the virus has changed
a particular amino acid, a building block for a protein,
which has led to a change in the spike protein
which attaches to human cells.
Now, when that spike protein changes very slightly,
the ability to neutralise that
and that interaction between the spike and the human cell
is reduced.
So that's the mechanism by which immunity is evaded.
And the mutation means it can get through a chink in the armour
of our immunity and still infect somebody.
So have we seen that E484K mutation arise more than once?
Yes, and so it's certainly present in the variant
that we're concerned about that's arisen
first in South Africa,
and the one that we detected in Brazil, and various others.
And are we likely to see more variants emerge
where their immunity to either our immune systems,
if we've been previously infected or if we've been vaccinated,
where that gives them an advantage?
Will we see vaccine-resistant strains?
The variants that are arising at the moment
may have a partial resistance to the vaccines we're using
in some parts of the world.
In the UK, I'm confident that the vaccines we have in this country
are fully effective against our current variant that's circulating.
However, what it means for the manufacturers of vaccines
is that they're going to be repeatedly looking
at the variants that are emerging and tweaking their vaccines
so that they remain effective.
The other big thing, of course, we worry about
with all these variants is, are they more likely to kill us?
What do we know so far? Yes.
There is one variant where we think that's the case.
It's not absolutely certain yet,
but there's growing evidence that the variant
circulating in the UK at the moment, the 117, the Kent variant,
is more lethal than other variants - by about 35%.
That number sounds very scary, but actually,
if you were to take a group of 60-year-old people,
and ten out of 1,000 might die as a result of infection,
what we're talking about here is 13 or 14 people.
Now, that's really key for them as individuals,
but it's not a huge leap.
OK, so 35% sounds like a lot,
but when you actually look at the numbers,
it's not a massive, absolute increase.
Just a few years ago,
a fast-mutating virus might have been a problem
for an effective vaccine programme,
but vaccines have changed.
So how does up-to-the-minute gene manipulation
help beat the virus at its own game?
230 years ago, Edward Jenner worked out
that he could prevent smallpox using the closely related
but less deadly cowpox virus.
This technique became known as vaccination -
from vacca, Latin for cow.
And it's because of this idea that we stand any chance
of defeating Covid at all.
The contents of this vial are one of the most
astounding success stories in modern science.
It is, of course, one of the new vaccines for Covid-19.
Each dose contains 50 billion life-protecting
particles of vaccine.
Vaccines are typically made from a virus
that has been weakened or killed.
Once vaccinated, our immune system remembers the shape of it
without making us ill.
And then, if we encounter the virus for real,
our bodies are primed to neutralise it.
Vaccines for measles and many other diseases
are made like this.
But in recent years, scientists have been rethinking
the way that vaccines work,
and they've come up with some really revolutionary approaches.
They all rely on the latest in genetic engineering
so that the genome of the virus is at the heart of the vaccine.
I've come to Oxford BioMedica,
and this is where the Oxford AstraZeneca vaccine
is being manufactured.
It's one of the new generation of vaccines.
This new generation is radically different
because you only need to know the genetic code of the virus
to start development.
One of the key scientists who helped design it
is only two miles down the road,
but researchers in this field need to be extra careful,
so I'm talking to Professor Teresa Lambe remotely.
So, to start designing your vaccine,
you didn't need a sample of virus?
No, we absolutely didn't.
We just needed to know the coding sequence.
The email came in late Friday, early Saturday -
that arrived in my inbox from a good friend of mine at the NIH.
And then there was more database updating over the weekend.
And I spent that weekend, myself and colleagues,
working on designing what we thought would be the most effective
part of the coronavirus to include in a vaccine,
and how to do that.
Within a few days of receiving the genetic code
for the protein spike,
Tess was using it to make the vaccine.
What we've done is, we've taken the spike protein,
and that's a small, tiny part of the virus -
the outside of the virus -
that allows the virus to get into our body and into our cells.
Only this spike code is needed to make a vaccine
that will prime the body's immune response.
The whole virus isn't required.
The spike's genetic code is then spliced into the DNA of a vector -
a biological container that transports
the viral genetic material into our cells.
For the vector, Tess used an adenovirus -
a mild cold virus which had been rendered harmless
by further genetic engineering.
The vaccine can then be injected into the upper arm,
where it enters individual muscle cells.
These cells read the genetic code for the protein
and create spikes on their surface.
The immune system identifies these strange-looking spikes
as foreign, and produces memory cells
that will remember this spike protein.
The vaccine can't cause an infection,
but it primes the immune system.
This army of memory cells will spring into action,
producing antibodies and T-cells, should it ever encounter
the virus for real.
So it's a bit like a Trojan horse.
Your body thinks that it's seeing an invading virus in your arm
and it mounts a really strong immune response towards it.
Over in Germany,
the Pfizer BioNTech team have used a different technique.
Like the Oxford vaccine,
they isolated the genetic code of the spike protein.
But instead of using DNA,
they used messenger RNA -
also found in a cell's nucleus -
and they inserted it into a tiny drop of fat.
Then, once injected, it creates immunity,
just like the Oxford vaccine.
So, by spring 2020,
both the Pfizer and the Oxford AstraZeneca teams
had finalised their vaccines. They'd made them.
You know, I cannot emphasise enough how quick that is.
Before Covid, the fastest a vaccine for a new disease
had ever been made and licensed was around five years.
Yet, in just nine months,
and after thorough testing on over 24,000 volunteers,
the Oxford vaccine was shown to be both safe and effective.
New-generation vaccines have an added advantage.
Because you don't need to work with the real Covid virus
under strict controls,
they can be quicker and easier to mass-produce.
AstraZeneca is collaborating with Oxford on the new vaccine.
Head of R&D here is Dr Mene Pangalos.
We're talking, for the AstraZeneca vaccine,
of potentially up to three billion doses,
or as close to that as we can get in 2021.
The manufacturers are all manufacturing at a scale
that they've never done before in their histories.
Another crucial benefit to using genetically engineered vaccines
is that there are new variants of Covid involving the whole time,
and they may be able to circumvent the vaccines
that we're currently using.
The one that we're most concerned about at the moment
is the variant associated with South Africa.
And as we see this spike protein mutating and changing,
we can very quickly adapt the sequence in the vaccine
to adapt to those new variants.
And that's a big advantage for these platforms,
because, as these variants appear, we can start to get
those new versions of the vaccines out into the population
as quickly as possible.
A new-generation vaccine for a dangerous variant of Covid
will be rapid to produce
because the genetic information for the mutant spike protein
can simply be slotted into the vector.
So they should be available in months rather than years.
I'm an infection doctor and I study viruses in the lab,
and even for me,
the technology that's being developed and now manufactured
in this building feels totally extraordinary.
Brand-new, the beginning of a new era in the way
that we prevent infections around the world.
Professor Eleanor Riley is an immunologist
from the University of Edinburgh.
Eleanor, it's very nice to speak to you.
The mutations -
if we didn't update our vaccines,
would mutations and new variants eventually render them useless?
I think we don't yet know how much capacity there is
in this virus to keep mutating.
So we know, for viruses like flu and HIV,
they have an almost infinite capacity to mutate,
to change and still to infect us.
I think, with this virus, we don't know how much flex
there is in the virus to keep mutating
and still be infectious.
And I think, until we know that, it's very difficult to know
how far this virus might mutate,
how far it might escape the vaccines,
and therefore how much we're going to have to adapt the vaccines
to keep up with it.
OK, so we're just seeing these new variants
because this is the first time it's spread
throughout the human population.
Yeah, we're watching this virus evolve in real time.
All the sequencing that we're getting is showing us how,
step by step, this is changing from an animal coronavirus -
and we don't quite know which animal -
into a human coronavirus,
one that is a much better fit for our cells.
And in a way, my feeling is we just need to let the virus
settle down a little bit, find out what is the best fit,
and then see if it keeps on mutating after that.
Do you think we're likely to get into a scenario
a little bit like we have with flu,
where we decide, as the scientific community,
what sequences we're going to plug into that year's vaccines
and there'll be an annual or biannual update?
I think, if that's the system we end up with,
I think it wouldn't be an absolute disaster.
But it's not just whether the virus mutates,
it's how long the vaccines protect you for.
And do they protect you against severe disease and death
for a long time, even if you might actually get a mild
or an asymptomatic infection and be able to transmit it?
I think it's quite possible that the vaccines may protect against
severe disease and death for much longer
than they protect against infection and transmission.
There's been a big discussion about the interval
between the first and the second dose.
And in general with vaccines,
leaving an interval beyond three weeks does allow
an increased immune response
compared to a very short interval, is that right?
Not necessarily increased,
but it seems, certainly with some other vaccines,
to induce an immune response of higher quality.
So when you have your first dose of vaccine,
you activate a whole range of immune cells,
some of which, quite frankly, are better
at doing the job than others.
And if you go back and boost within three or four weeks,
you boost all of those cells.
But if you wait 8 to 12 weeks, some of the not-so-good cells
tend to die out.
And so when you go back in, you only tend to boost
the very high-quality cells,
and that means at the end of that process, you've got
a much higher-quality response than if you went in earlier.
But you're always balancing what is the risk of waiting longer
if you haven't got a full immune response versus the benefits
of waiting longer.
What's the future for this virus in terms of eradication?
Some people are saying that might be possible.
The virus is on a bit of a tightrope.
If it changes enough to avoid antibody response,
it may no longer be able to bind to the receptor on our cells.
So really what we're trying to understand is how much tolerance
there is in the virus being able to be still infectious and yet
still mutate to avoid our immune system.
And I think we don't yet know where those levels of tolerance are.
OK, so that's the trade-off.
A mutation that completely avoids the immune system is of no use
if that mutation in the spike protein
means it can't bind to our cells. Exactly.
That makes sense.
We hope the vaccination will prove to be a decisive weapon
in our fight against coronavirus.
But until that point, understanding how the virus spreads
around the country is vital if we are to keep
infections under control.
Dr Guddi Singh is on the trail of an airborne mystery.
In the summer of 2020, an international flight carrying
49 passengers landed in Ireland.
What no-one knew at the time
was that 13 of those passengers would later test positive
for Covid-19.
What happened next is documented in this academic paper.
It reveals how the virus spreads through the population
and highlights an often overlooked factor which could help us
to get on top of the spread of Covid-19 and keep it that way.
From the very beginning of the pandemic, air travel helped
the virus spread quickly around the world, and scientists
relied on mathematical models to understand the dynamics
of coronavirus transmission.
By now, we've probably all heard of R, the reproduction number,
which represents the number of people one infected person
will pass the virus onto.
The baseline reproduction number for Covid-19 is around three,
which means that without any control measures in place, one infected
person will infect three others who will go on to infect
three more and so on.
But the R number is just an average.
It explains what happens in a whole population.
It tells us nothing about what happens to individuals.
When scientists investigated the Irish flight outbreak,
a combination of contact tracing, testing and DNA sequencing revealed
something very different to what the R number
would have predicted.
Most of the infected passengers hadn't passed the disease on
to anyone else, either during or after the flight.
Instead, all of the onward transmission, 43 cases,
stemmed from just five passengers.
This is anything but the even distribution the R number suggests.
So, as well as R, epidemiologists use another key measurement
of transmission, the lesser-known K factor.
The K number describes how much the disease clusters, it measures
the difference in how many people each person with coronavirus
infects, and it shows us how much of the spread
is down to the super-spreading few.
By analysing outbreaks like the one in Ireland,
scientists have calculated the K number for Covid-19.
A small K number means that most of the transmission is caused
by a small number of people, while a large K number means every
infected person contributes roughly the same to the spread
of the disease.
Covid-19 has one of the lowest K numbers of any infectious disease,
and it means that as few as 10% of infected people
may be responsible for as much as 90% of all transmission.
But infected people are very difficult to study.
So to try to get a handle on the phenomenon, super-spreading
expert Mark Woolhouse examined pigs.
And we found that some pigs simply produce more virus than others.
Some pigs actually didn't infect any other pigs at all.
Others were capable of infecting four, five or six other pigs,
so there was a very big variation in how much infectivity
there were in these different animals.
And so, do we know yet if there is anything that is biologically
different, that means that people become super-spreaders?
Well, that's the absolute key question.
The research is ongoing and differences in our individual
biology, like the thickness of our saliva, how violently we cough
or even how loudly we talk may play a part.
But what's more likely to be a factor is the stage
of our infection when we meet another person.
So the most infectious period is typically the 24 hours either side
of first showing symptoms.
Viral load is high in the upper respiratory tract at that time,
so there's every possibility that a person will be highly
infectious at that stage of the infection.
For epidemiologists like Mark, it's all about where these infected
people are and what they're doing.
In any case, the individual's contribution to this only
materialises if they are making contacts, if they're in a setting
where transmission is possible.
So it is about the epidemiological context of this.
And so for that reason, I prefer not to talk about super-spreaders,
but I prefer to talk about super-spreading events.
A low K number could work in our favour.
If we can identify and target areas of high risk for super-spreading,
it should be easier to prevent.
And because not everyone transmits the virus, it should be harder
for an outbreak to take off.
I'm meeting Dr Adam Kucharski from the London School of Hygiene
and Tropical Medicine.
Hi, Adam. Hi, how are you?
Look, we know that super-spreading events happen, but is there anything
that we can do to try and stop or isolate them at all?
So, one thing that can really help is how we structure contact tracing,
incorporating that knowledge of super-spreading
into how we approach that.
So can you just explain to me how contact tracing works?
So there's two components to it.
I think all of us are familiar with the basic idea of contact
tracing, what we call forward tracing, where if you have a new
case appear, someone with symptoms gets tested,
has come down with Covid,
you look at all the people that they've come into contact with
and they potentially might have infected,
then you quarantine those people.
And so if one of them turns out to have been infected,
they can't then go on to infect others.
This is called forward tracing.
But in countries like Japan and South Korea, they also routinely
work backwards to see if they can uncover these clusters of infection
and stop further transmission.
So if you go backwards and look at the events that initially
infected them, that's likely to be a super-spreading event,
which means that there's probably quite a few other people
who were infected at this event who might not know it.
The theory is that the person who gave you the virus will also
have infected other people.
So by looking back, we'll soon get to the source of the outbreak,
the super-spreading event,
and uncover previously undetected cases.
So do we know what added benefit backwards tracing actually adds?
Yes, we've estimated in some modelling that in the two weeks
after one of these initial cases appears, if you add backward tracing
on top of forward tracing, you can potentially double the number
of onward transmission events that you prevent.
Covid-19 is an insidious and unpredictable disease
because hidden super-spreading events play such an important role
in its transmission.
But understanding K is only half the battle.
One of our best hopes for dealing with this disease is implementing
our knowledge and with fast and effective contact tracing
to catch cases and clusters before they have a chance to spread.
It was recently announced that a surge in testing
is going to be introduced to try to help us all get back
to a more normal way of life.
Up to 400,000 lateral flow tests are planned
to be distributed every day.
So it looks as though testing is going to become a big part
of all of our lives as we start to go back to work,
go back to school and to travel with more freedom.
Now, there are two main types of test.
There's the polymerase chain reaction or the PCR test,
and there's a lateral flow test.
Both tests analyse samples of mucus taken from the nose
or from the throat.
The PCR test looks for fragments of the virus's genetic material.
It generally needs to be sent to a lab.
This is a lateral flow test.
It can give you a result in a matter of minutes.
Now, both tests, PCR and lateral flow,
either give you a positive result or a negative result,
but it's vitally important
that everyone understands what that actually means.
Now, this graph shows an important difference between the two tests.
There's time on the X axis, viral level on the Y axis
and the white line is the level of infection in the body
and the grey shading in the middle
is the period of time
when you are likely to be infectious to other people.
Now, the lateral flow test
is only able to detect virus
in this period here,
whilst the PCR test can detect virus both earlier and for longer.
But what's also really clear from this graph
is that there is a blind spot
for both tests at the beginning.
It's possible to get a negative result
even if you've been infected already.
So both tests only tell you about whether you are positive
at the moment they are done.
You might become infectious days, hours, even minutes later.
But there is an additional thing that everyone needs to understand
about the lateral flow test.
When you get a positive result,
you are very likely to be infectious.
You must isolate and stop spreading the virus.
But these tests miss a significant number of Covid cases
when used in the real world.
And what this means is that if you have a negative result
from a lateral flow test, you may still be positive, even infectious.
So you have to keep acting, as we all are,
as if you might be infectious,
even if you feel well.
So a positive result should be taken seriously.
A negative result means you should not change your behaviour at all.
Testing individuals can be time-consuming
when we have so many people to test.
One ingenious way of gathering more data
is being trialled at the moment -
the continuous sampling of our sewers.
When someone has an infection, billions of virus fragments
are shed in their urine and faeces,
and these get washed into the sewers.
So the plan is that if a particular treatment station
sees a surge in levels,
they can alert the local authority to respond rapidly
with a targeted testing programme and hopefully stifle any outbreak.
Currently, the numbers are telling us
that while we are some way off the end of the pandemic,
thankfully we do seem to be coming out of the second wave,
and there's more good news.
Statistics on hospital treatment
show that tiny changes can add up to big wins.
And they give us another reason for cautious optimism.
Incredibly, the risk of dying in hospital from Covid
has more than halved,
falling from 35% to around 15%.
These amazing improvements
are, in part, thanks to a number of treatments
that on their own might seem insignificant.
Put together, they make a big difference.
You know, a year ago, this was an unknown disease.
Much of what we were doing was educated guesswork.
But within just a year, we have figured out so much
about how to treat patients with this disease.
This is University College Hospital in London, where I work,
and where my colleague, infectious diseases consultant Dr Sarah Logan,
has been battling the disease from the beginning.
A decision whether someone needs to come into a hospital
is around whether someone needs support for their breathing. OK.
And sometimes we need to give them a mask of oxygen.
At the start of the pandemic,
far more patients were put on ventilators -
an invasive procedure needing sedation
and a breathing tube inserted down the throat.
But now that's changed.
A type of breathing support called CPAP -
continuous positive airways pressure -
can prevent the need for such invasive ventilation.
There's a tube going to a machine
that is blowing oxygenated air hard at the face.
And what that means is, the air is forced down into the lungs
and it slightly inflates them.
And that has two effects -
it pushes oxygen into the body,
but it also pushes fluid out of the lung tissue and keeps it inflated.
A study in the north of England
showed that using CPAP early in the treatment of some patients
may also increase survival.
Of course, the sickest patients
will still need to go on intensive care,
where more remarkable discoveries are making a huge difference.
Mark Vargas is a senior critical care charge nurse.
Let's get ready.
You've aspirated...?
Mark and his colleagues have found
that lying critically ill patients on their stomachs, or proning,
has made a significant difference to survival rates.
A proning team consists of six people,
with one leading the team
and one holding the airway on top.
Before Covid, we'd do this maybe two or three times in a year.
Oh, really? OK. Yeah. Now you're proning
three patients daily in one room.
Daily, yeah, and there's more to be proned in the other bays. Really?
Proning patients like this can pull out their breathing tubes.
The expert team must take exceptional care.
Proning seems to help the sickest patients
because lying on their back all the time
can make fluid build up in the rear of the lungs
and they can be compressed by other organs.
Putting patients on their stomachs can relieve this
and allow better oxygenation of the blood.
I mean, there's such skill,
but that is such a risky thing to do to a patient
if you don't know exactly what you're doing.
And watching that,
that for me is the pinnacle of what goes on here.
Recovery rates in ICU have greatly improved.
In one study, survival improved
from 58% in March 2020
to over 80%
in June of the same year.
Part of that improvement is thanks to the advances in nursing care.
And some of it is because of a greater understanding
of how to treat the disease with medicines.
The steroid dexamethasone has been used for decades.
It broadly suppresses the immune system
and it can reduce the overall risk of death from Covid by up to 17%,
chiefly benefiting those patients on oxygen.
Another anti-inflammatory used to treat arthritis
has recently been shown to prevent one death in 25.
It sounds like a small gain,
but taken together with all the other improvements in care,
it makes a big difference.
Has there been sort of one giant leap,
or is it lots of little changes?
Without doubt, it is little adjustments
to lots of different things.
I feel, with someone who I thought
might not have survived back in March,
I feel we've got so many more tools in our cupboard
to help get them through it.
The improvements in survival with Covid-19 that we've seen
over the last year are largely
because we are optimising all the different aspects of patient care,
and that really is a tribute
to every person that works in this building.
There's still an unfolding tragedy, of course, but we are now able
to save many, many more lives.
We may be coming off the peak of the second wave,
but that means that many of us who have had the infection
might be worried about long Covid.
It's one of the more surprising and unwelcome things
about this infection.
I got Covid in April and it left me with a heart arrhythmia
and fatigue and exhaustion for many months afterwards.
Dr David Strain is the BMA's lead on the NHS's long Covid task force.
David, thank you very much for coming in.
Are my symptoms typical of the kind of things that you're seeing?
Your symptoms are very typical.
We do see many patients who present with these cardiac problems
or with breathing problems and then a fatigue.
There's two real types of long Covid.
There's long Covid that can be attributed
to a really bad case of Covid in the first instance,
so they're the people who ended up in ITU,
they're the people who got pulmonary scarring,
they might have had small clots in the brain
or small clots in the body,
and they've left them with long-term consequences afterwards.
But then the surprising group that's come out of this
is a group of individuals like yourself
who didn't get particularly bad Covid,
but we're getting many people who, two to three months later,
are still left with this chronic, debilitating fatigue. Really?
So even if you haven't been in intensive care,
you haven't been severely short of breath,
you haven't had that kind of severe, immediate organ damage,
you can still have very, very protracted consequences?
Absolutely. And if anything,
we're seeing it more common in the younger patients,
the fitter, the very active,
the ones who may have got over the initial disease very quickly,
but then have been left with these long, debilitating symptoms.
We've got some patients who caught Covid back in March
and still are not able to function for a full day.
What we think is happening is,
the virus is affecting the mitochondria of the cells.
So, the mitochondria of the cells are...effectively
it's the battery that every single cell has that keeps it charged,
that keeps it able to do things.
Long Covid is effectively like having a run-down battery.
We've all seen a smartphone
that's had three or four years' worth of use
and it will die in about 50 minutes
after you take it off the charger.
Long Covid leaves your cells in exactly that same position.
Just the walk to the kitchen,
you'll start to feel tired and exhausted.
I definitely felt that. When I woke up in the morning I'd think,
"Great, I can attack the day. This is going to be fine,"
and I'd ride my bike to work and be shattered by the time I got there,
almost in tears, I was so tired.
One of the key things that we're recommending
is that people stay within their energy envelope.
So if you know that you are going to be exhausted
after you walk a mile, stop 200 yards short,
sit down, rest, let your battery recharge naturally.
Is there anything you can do
to reduce your chances of having long Covid?
One of the common features
in our studies of people who've got long Covid
is that they're people who,
when they caught it in the first instance, tried to work through it.
They tried to say,
"Oh, it's only a mild disease, I'll shrug it off, I'll get on."
And the result is
that they've been left with much more lasting consequences.
So the one piece of advice, I would say,
if anyone tests positive,
if anyone's got even the mildest symptoms, take it easy,
go easy on yourself,
because the more chance you get to recover today
means the better you will be over the next few months and few years.
This has perhaps been underemphasised,
how important it is, even if you have a mild case of Covid,
that you rest and take the time to recuperate
maybe much longer than you would naturally be inclined to do.
Yes. If you do catch Covid, you need to take it easy.
You need to sit back and relax for two, maybe three or four weeks
before you start trying to re-engage and do things
as you would normally have done previously.
Before this coronavirus came along,
you had worked on chronic fatigue syndrome, on ME,
and other things that we sort of associate with viral infections
that affect people for a long time.
Has the emergence of long Covid
changed the landscape for people with those conditions?
It's a silver lining to this whole outbreak
that people who've been shouting about ME and CFS
for the last 20 years are suddenly being heard.
One of the studies that we're planning on doing
is going to be directly comparing patients with long Covid,
patients with chronic fatigue syndrome,
because we think there are going to be some similarities.
Now, the two main areas that we're looking at
are in the mitochondria,
the batteries that we spoke about
that we know are affected by long Covid,
and then the other place that we're interested in
is the microcirculation, the smallest blood vessels,
the ones that are responsible for delivering the oxygen
and the nutrients and the hormones to your tissues.
And the hope is that as we develop a treatment for long Covid,
that can then carry over
and we can then start treating these people who've had CFS or ME
for the last 20 years
and have been left with what is a life-changing physical illness
that they've struggled
to even have accepted as a disease in its own right.
So interesting. David, thank you very much.
The story of Covid has so far been full of twists and turns
and has lasted longer than any of us wanted.
But so far, science has provided us with an impressive armoury
with which to fight the disease.
Can it also provide an answer
to the biggest question of all -
when are we going to get back to normal?
This week, we've seen the first potential
timelines laid out for the lifting of restrictions.
But with so much uncertainty still ahead,
can we ever envisage a time when we will be totally free of the virus?
An answer to when that day might come could lie in mathematics,
and in this fairly simple formula.
It's all about H, the herd immunity threshold.
That's the percentage of people who must be immunised
in the population to stop the disease from spreading.
And we can work that out
if you know these two things -
R0, the reproduction number,
which is how easily the virus spreads
if there are no restrictions,
and E, vaccine efficacy, a measure of how well the vaccine is working.
Let's plug in numbers for coronavirus.
We'll assume the baseline R0 is 3,
and we'll use an average efficacy
of the two vaccines currently in use, around 79%.
This gives a figure of 84% of the population that need the jab
to achieve herd immunity, about 56 million people.
Now, we've been immunising 2.5 million people a week,
and at that rate we should reach herd immunity by November 2021.
But our figures make huge assumptions
that are tricky to pin down in the real world.
Let's leave the reproduction number, R0, for the moment
and turn our attention to efficacy.
So efficacy is a measure
of how well a vaccine can protect a person
from an infectious disease, in this case Covid.
If a vaccine in a clinical trial is shown to have an efficacy of 50%,
this roughly tells us
that we can expect those people who are vaccinated
to have a 50% reduced risk of becoming sick
compared to an otherwise similar unvaccinated group of people.
So if I understand that correctly,
it's not as though the vaccine
just switches off our risk of getting the disease,
it's more that it reduces the risk of us getting the disease,
it kind of dials it down. Yes.
What we now say about the AstraZeneca vaccine
is that it reduces disease.
And what we've also seen is it reduced hospitalisations,
so how severe the disease is
and whether you need to go into hospital.
However, the clinical trials that were done for all the vaccines,
or the majority of vaccines, did not look at transmission,
whether you can still become infected,
you don't get severe disease,
but you could pass that infection on to someone else.
Early indications suggest the AstraZeneca vaccine
may reduce transmission by around 67%,
but more robust data on all the vaccines is needed.
Expressing vaccine efficacy as a single exact figure like this
is useful for illustration,
but it's a little bit simplistic for real life.
It assumes that the vaccine protects equally well
against infection as disease
and that the vaccines will be just as effective in real life
as they were in clinical trials.
To get an idea of how even a small reduction
in the real-life vaccine effectiveness affects our formula,
let's see what happens if we reduce the efficacy figure
by just a couple of percent.
So instead of our 79%, let's use 77%.
If we do that, what we'll see
is that the percentage of people who have to be immunised
to reach herd immunity goes up from 84%...
..to 87%.
And small changes matter.
This could delay when we get back to normal by weeks.
And then, of course, there's R0, the reproduction number.
At the beginning of the pandemic,
scientists thought one infected person
would on average infect three others.
They'd go on to infect three more,
and so it spreads through the population.
But epidemiologist Mark Jit has found
that the increased transmissibility of new variants
could have changed this number.
We knew that the proportion of cases
with this variant was growing in some parts of the UK.
So what we did then was to take this data and say,
"Actually what set of parameters for this virus is consistent
"with what we're seeing in the world?"
And we found that the new variant was about 50% more transmissible.
We started off with a reproduction number of three,
so 50% more of that would be around four, four and a half?
It's difficult to say,
because we haven't seen how fast this variant spreads
without any restrictions at all.
But I think our best guess
would be about four, four and a half, yep.
Let's be optimistic and use a baseline reproduction number of four
and let's keep our efficacy figure at 77%.
What you'll see happening then
is that our herd immunity threshold leaps up from 87%...
..to 97%.
But will we ever be able
to vaccinate that many people in reality?
So, Roy, herd immunity actually works really well, doesn't it,
with some diseases?
It works very well.
I mean, the best example in the United Kingdom
is the introduction of measles vaccination roughly in 1967, '68,
and slowly over a period of a few decades,
we built up sufficient immunity in the population
that measles went from 800,000 cases a year
down to less than 1,000 cases a year.
We eradicated the transmission of measles in the community.
In Britain, our success against childhood measles
shows that achieving very high vaccination levels against Covid-19
might be possible.
But there's one other real-world thing to consider.
We've got new strains coming into play, so it's important
to recognise that the duration of immunity
for this coronavirus vaccine set is unknown at present
and we will only find this out in subsequent years.
What I do think is that we will eradicate serious morbidity
and mortality, and hopefully it will become one of these things
where every year, like influenza,
you have a vaccination against it.
Protecting those at risk with vaccines may allow us
to live with the virus,
even without herd immunity.
And as we've heard this week,
this protection could help us emerge from many of the current
restrictions as head towards the summer.
What we all want is to be able
to see and be with each other again safely.
The way to get there is to make sure
that population immunity is as high as possible,
and vaccination means that we can all play a part.
The pandemic continues to be a human tragedy.
At the same time, our scientific ingenuity has allowed us
to make great strides in understanding
and fighting the virus.
Ever since the structure of DNA was revealed,
the idea of genetic engineering has been controversial.
But now our ability to understand
and manipulate life at its most fundamental level
has paid dividends.
And it's because of this capability
that the innovative vaccines have been delivered
and that globally, millions of lives will be saved.
This knowledge is a cause for some optimism,
not just about the end of THIS pandemic,
but about those that we will face in the future.