Dec. 30, 2020 -- Colorado confirmed the first known case of COVID-19 in the United States that stems from a variant of the coronavirus that emerged in the U.K., according to NBC News.

Colorado Gov. Jared Polis announced Tuesday that the case involves a man in his 20s who didn’t have a recent travel history. He was working at a Good Samaritan Society assisted living facility in Simla, which has had an outbreak over the past few weeks.

“There is a lot we don’t know about this new COVID-19 variant, but scientists in the United Kingdom are warning the world that it is significantly more contagious,” Polis said in a statement.

“We will closely monitor this case, as well as all COVID-19 indictors, very closely,” he said. “We are working to prevent spread and contain the virus at all levels.”

Health officials believe they may have found a second case of the variant at the Good Samaritan Society facility, according to CNN. Both men were temporarily working at the facility due to staffing shortages after the outbreak and are not regular staff.

“The state health department has deployed a rapid response team to the assisted living facility in Simla to test residents and staff,” Dwayne Smith, the county health director, told CNN.

Doctors Whyte and Topol Discuss COVID-19 Vaccine Status and Future Direction With FDAWebMD's Chief Medical Officer, John Whyte, MD, and Eric Topol, MD, Executive VP, Scripps Research, Editor-in-Chief, Medscape, speak with Stephen Hahn, MD, Commissioner of Food and Drugs, FDA, and Peter Marks, MD, PhD, Director, Center for Biologics Evaluation and Research, FDA, to discuss COVID-19 Vaccine Status and Future Direction With FDA.1791


DR. JOHN WHYTE: Welcome,


I'm Dr. John Whyte, Chief

Medical Officer at WebMD,

and welcome to Coronavirus

in Context.

We're going to do the show

a little differently today.

I'm delighted to be joined

by a co-host, someone many

of you know, Dr. Eric Topol, who

is the Editor-in-Chief

of Medscape.

And our guests today are Dr.

Stephen Hahn, the Director

of the Food and Drug


and Dr. Peter Marks,

the Director for the Center

for Biologics Evaluation

and Research at the FDA.

Gentlemen, thanks for joining



DR. STEPHEN HAHN: Thank you,


DR. PETER MARKS: Thank you.

DR. JOHN WHYTE: Well, Eric and I

had a coin toss and I won,

so I get to ask

the first question.

And I'm going to give it to Dr.


And I want to ask you what has

been on many people's minds.

A lot of folks have been talking

about how the data is so

compelling, in terms of safety

and efficacy.

So then the question becomes,

if that's the case, why

an emergency use authorization

and not a full approval?


it gets to the heart

of the issue of what an EUA

emergency use authorization is,

and that's a special authority

given to us by Congress

after 9/11 and the attacks

to expedite medical products.

And really, just very simply,

the major difference

between an EUA for a vaccine

and a biological license


is the amount and the complexity

in the manufacturing data

that we would need to seeing

a biological license


as well as the duration

of follow up for safety.

But I want to make one thing

clear, as Dr. Marks and his team

were very clear in the guidance

that we issued, both in June

and in October,

that we needed to see very

compelling evidence.

And the actual term we used

was "clear and compelling

evidence" of safety and efficacy

from at least one

randomized clinical trial

for a vaccine.

So those criteria are very

similar to what we would use

for a biological license


So in terms of at least

the initial assessment

of efficacy and safety, very

robust data we received, very

similar to what we would sort of

expect from a biological license


And what we'll do moving forward

is work with the companies

for that full application,

get additional manufacturing


but also get additional safety

and follow up data.

And Dr. Marks and the CDC

have put

in a terrific post-marketing

pharmacovigilance surveillance


to pick up any additional safety

issues that might arise.

DR. ERIC TOPOL: Well, you know,

the EUA and the two vaccines now

out there in the US

is really extraordinary.

So I want to start off just

by congratulating you, Steve

and Peter, and what you've done

over the last couple of months

is just extraordinary.

I mean, considering all

that you're up against--

that is, we had nothing,

and then you also had all sorts

of external, unnecessary


And you were basically

in a fishbowl

to try to get this thing


So I think it's extraordinary,

and I know how hard you all have

been working to get where we

are, which is just momentous.

So it doesn't go

without appreciation.

And I want to just say,

on behalf of all

the medical community,

and I'm sure the public, to see

the FDA--

this is

their crowning achievement--

transparent, everything vetted

with the external experts,

internal at the FDA.

I mean, it's just remarkable.

Now, the EUA was tightened

along the way, I think back

in October.

And then maybe, I don't know,

Peter or Steve, you could just

give us some insights

because that was

an important step that you all

took to make sure that you got

where we actually wound up,

which is two complete trials

which demonstrated replication

of such extraordinary efficacy.


the issue here is that we tried

to be very clear about what we

needed to see.

And it's something that we've

been thinking all along,

but we thought it would be very

important to make clear

that if we were going to have

data on these vaccines that made

people feel comfortable using


they needed to have

the kind of safety data

that allowed us to have


that the great majority

of adverse events

would have been seen.

And we know that it takes--

from studies that have been done


it takes in general about 42


when most of the adverse events


And if you look

at various studies that have

been done, two months median

follow up allows you to get

the large majority

of adverse events associated

with vaccine administration.

It's true that there can be

some later events that come

along, but the great majority

occur within that period.

So by putting that condition

there, it allowed us to give

people confidence

about the adverse events

that we might see.

But it also allowed us to know

that these vaccines didn't just


some transient immune response,

that at least there was

a median duration

of immune response of two

months or longer.

And that was another piece

of this.

Because you could imagine,

especially when using

new classes of vaccines

that you could see

some unexpected things.

So I think that combination

of safety and efficacy,

a median two months

follow up for the population was

something that allowed us then

to have a confidence in what

the output here was.

DR. ERIC TOPOL: Yeah, well, you

got the full efficacy endpoints

for both the Pfizer, BioNTech,

and the Moderna trial.

So that was just--

everything was just remarkable


And another point that is,

I think that a lot of people

don't understand

the medical community

is a contribution that you made

with respect to this concept

of Operation Warp Speed.

My understanding, Peter, is this

was your brainchild,

and you're a Star Trekkie.


And that you had this kind

of incredible--

DR. JOHN WHYTE: I don't know

he's going to take credit

for the name.


Well let's hear that.


DR. ERIC TOPOL: --crazy idea

that we could all do this pretty


Can you tell us

about this eureka moment

about what turned out

to be Operation Warp Speed?

DR. PETER MARKS: Yeah, Operation

Warp Speed started

from something that we started

internally at FDA, which was

Project Warp Speed, which was,

how could we internally speed up

the regulatory advice

that we would give to product


And then it gradually morphed

into something more when it

became apparent that a number

of the manufacturers,

the vaccine manufacturers

were talking about timelines

that were a little bit less

aggressive than we were

comfortable with, in terms

of when they thought they would

have a vaccine.

I mean, there was timelines

being talked about of not having

a vaccine until summer of 2021.

And when looking at modeling


we were able to see that that

was not really going

to be a great thing, because we

knew, we could already predict

that we were going to have

issues this fall and winter.

So that led us to kind of feel

the need to escalate this

and have conversations

with the companies

and ultimately snowballed

into Operation Warp Speed.

And thanks a lot to Commissioner

Hahn for supporting moving ahead

with this

and advancing this up

through the secretary.

So I'm very

grateful to Commissioner Hahn

for his leadership

in supporting this.

I think it helped wake us

all up as a community

that we have to do something,

and I'm glad that it took off.

DR. JOHN WHYTE: I do want to ask

you, Dr. Marks, a little more

about the safety data

and efficacy data.

Because even when we talk

about Operation Warp Speed,

in some ways we should be

celebrating innovation.

But people are concerned,

because they're not hearing

enough about how we didn't cut

corners, how we were

able to innovate and no steps

were cut in terms of safety

and efficacy.

But you addressed the issues

of safety,

that it's

consistent with other studies,

that most adverse events

or serious adverse events

we're going to see in 60 days

and we're continuing to evaluate


But on the efficacy side,

I wanted to ask you,

because there's been an argument

by some that it wasn't the best


We're looking

at symptomatic infection

at a certain number of days,


You know, should we be looking

at different types of antibody?

Should we be looking at and

other outcome measures?

And I recognize the studies are


But can you explain

to our listeners

about the efficacy data

and how those endpoints were

chosen and were

the correct endpoints

in your decision-making?


the idea here of using

a clinical endpoint of disease


that you could come

to reasonably,

in a reasonable amount of time,

I think it was a very--

these were event-based trials

based on that,

and I think it worked out

actually quite well.

In general, what we've seen

with vaccines is if you can


mild to moderate disease,

you generally have

a beneficial effect

on severe disease.

I mean, think about it

with influenza vaccine.

That's how it works there too.

Even if you're not completely

protected against flu by flu

vaccine, you generally can show

an effect of actually lessening

severe disease.

The same thing for any number

of other diseases.

So although some would say,

well, we should have had a more

severe disease endpoint,

some would have said,

oh, well, you haven't done

an asymptomatic carrier study,

the problem was to try

to actually swab people's noses

daily for 30,000 people, that

was going to be

a real challenge.

So I think what this was, was

a balance of a somewhat

pragmatic approach with what I

think is a very valid endpoint,

a disease endpoint, which I

think we'll follow up.

Now the most important place

to build next

is, can we see

that their immune correlates

of protection from the blood

samples that have been obtained

that help us

understand for our next trials

moving forward,

do we have an immune correlative

protection so we don't have

to use clinical endpoints?

DR. JOHN WHYTE: And what

is that immune correlate

that you're looking at?


the immune correlates that we'll

look at were obviously

the antibody levels

and in some cases will be

the T-cell, the immune responses

that we're seeing,

whether it be a T-cell response

or a humoral immune response

will be hopefully things that

will correlate with protection


DR. ERIC TOPOL: I wonder, Steve,

I can go back on the timing

issue, because one of the things

that I think a lot of people

don't realize

is this hyper accelerated

schedule from a sequence

of the virus January 10th

to the beginning of phase I,

II trials of Moderna in March,

and then the seamless-- you

know, you don't stop after phase

I and II, you go to phase III.

Everything is moving.

And then, on the other hand,

critique that, oh, well, how

come the UK got to get

their approval, whatever, a week

or 10 days earlier?

Can you speak to-- you pulled

out all the stops to move this

so fast.

And then you get from the flak

about the UK getting a review


Can you kind of balance this out

for us?


Really, really terrific


So you really nailed it, Eric,

that Peter and his team,

what they did-- worked very

early on with the developers

of vaccines

to reduce the time

in between the different phases,

if you will, of development,

to compress that time schedule,

not to cut corners

in the development,

but to go seamlessly from animal

studies into phase I

and then phase I to phase II

and then phase II,

and then of course

had to wait for the events

for phase III.

And on the side

of the regulatory assessment,

working on a rolling basis

with the companies,

having frequent communications

also significantly helped reduce

the time that we would need

with respect to review of this.

So I'm going to sneak this

up front.

We at FDA did not see this

as a competition

among regulatory agencies

around the world.

And I can't speak to what

any other regulatory agency

looked at.

What I can tell you is that Dr.

Marks' team, in the past,

for an application of this size,

let's talk about Pfizer,

it would normally take three

or four months to fully review

that and vet all the data.

Remember, FDA,

unlike any other regulatory

agency goes line by line

in the data.

We do our own number crunching.

We do

our own statistical analysis.

Eric, you know how this is,

and John, in medicine, if you

don't verify and actually do

your own analysis,

you're relying

upon other people's assumptions

and the way they look

at the data.

We have to get this right

for the American people.

So we did that.

And so when people ask questions

about pregnant women, people who

had renal failure

and other issues,

we were able to look at the data

and come back with answers

or not, and say, look, there's

not enough data there.

If you look at the issue

around allergies,

that was something that we

looked into in the data

and we could provide

great confidence about what

the data

from the clinical trials showed.

So this is what distinguishes


And I am incredibly

proud of the heroic efforts

that the people at CBER did.

The reviewers and Peter--

I mean, three weeks, basically,

for the Pfizer BioNTech vaccine

application, and 2 and 1/2 weeks

for the Moderna application,

really record time,

but at the same time,

did their incredibly thorough


They are truly heroes.

DR. ERIC TOPOL: Well, you know,

I have to say, I've been doing

clinical trials since the 1980s,

making me very old,

but, you know, I've never seen


These are the two largest--

a couple of the largest trials

in medical research history,

and 74,000 people.

It's really quite extraordinary

how you got all this done so


Now you set a new standard which

will not be easy to replicate.

DR. STEPHEN HAHN: No, that's

true Eric.

And, you know, I think

the other part of this--

the other thing that should

instill confidence

is that two trials, 30,000,


when you look

at the average trial

for a vaccine

that Dr. Marks and his team

has reviewed in the last couple

of years, it's in the low 20s.

I think it's 21,125

is the average.

So really a lot of data.


DR. JOHN WHYTE: Let's talk

about children.

I asked Dr. Fauci about

that yesterday.

And as you know,

Dr. Hahn and Dr. Marks, even

in my time at FDA, we would say,

children are not mini-adults.

So we don't necessarily

extrapolate findings in adults

in children less than 12,

recognizing that there are

changes based on age.

So as we talk

about the reopening of schools,

as we talk


the symptomatic and asymptomatic

journey of the disease

in children,

tell us your thinking, in terms

of what needs to be done

in terms of studies in children,

whether that needs to be

a priority,

or we have enough information

and we should focus resources

on the adult population.

DR. PETER MARKS: Really this

is a great question.

And we have to study children,

because the only way we're going

to stop the COVID cycle

is to immunize enough

of the population

that we don't have individuals

that are mainly

asymptomatic-- although children

do get COVID-19


but we're going to need to stop

the spread.

So we're going to need data

in children, and we're going

to need data that we can trust.

And that means we're going

to have to do clinical trials

in the manner in which we've

done them for other vaccines,

which means we'll do age


So in the very near future

we'll probably see trials

starting where you'll see 12

to 15-year-olds enrolled

in the first cohort, followed

by 7 to 12-year-olds,

followed by younger children.

And those will be

critical to have those studies,

especially because it's not

totally clear

that these vaccines will be


safe from extrapolation

in those younger populations,

because we do see

this inflammatory syndrome,

and we want to make sure

that we're not going to see

something there that is


So we do have to study them.

We can't treat them

as mini-adults.

And those studies will get


Now the hope too is that we'll

be able to use some of what

we've gained, in terms

of immune cohorts of protection

to accelerate that study.

But we need the safety data

in those populations for sure.


of the things that's come up now

in the post-EUA is

the single dose story.

And so, as you both know very

well there was a sign

of efficacy that was somewhat

anticipated starting about

10 days after the first dose

in both the trials, Pfizer

and Moderna.

And there are some people

advocating studying that,

and more worrisome are people

advocating that you should just

take the one dose because then

you won't have to deal with side

effects or logistics

or whatever.

Can you speak to this?

Because I think

there are some real concerns

about potential drop off

of efficacy.

And it's the only thing that was

tested was two doses.

DR. PETER MARKS: You know,

this one, I just--

this is something that--

I understand the temptation


But we spent all this time

and effort doing really good

science, right.

We actually tried to do

the science right, and then, oh,

we're just going to-- we'll just

throw it all out and just--

DR. JOHN WHYTE: One's better

than none, isn't it, Peter?

One's better than none.


Well, one's better.

But actually there are

social scientists that will tell

you that one could be worse

than none if what one does

is makes you throw out all

of the protection you're taking

and rely on something that might

not be true.

So let me just tell you why you

need the science.

We know that there's a trend


it looked like, right,

that there was about 50%

efficacy between dose one

and dose two with the Pfizer

vaccine, for example.

And the problem is that nearly

everyone got both doses

of the vaccine.

So we don't know if after one


you could have 50% protection

but maybe it only lasts for two


DR. ERIC TOPOL: Or less, yeah.

DR. PETER MARKS: And so we just

don't know what that answer is.

So I think, as Dr. Topol noted,

it's not crazy to actually study


It's a reasonable question

for study.

But to just go off and do this,

I think it's--

I don't want to say something

too critical, but I think it's

not exactly responsible.

Because people need to know--

the reason why I see health care

providers sending me

pictures where they're smiling,

despite the fact that you can

see it hurt that the vaccine

went in or they felt kind

of crummy the next day,

is because they know

that they're doing so

with the risk

of that discomfort, balanced

by a benefit of a vaccine

that they know to be

95% effective.


DR. PETER MARKS: And that kind

of calculus gives people


If you have something

that, well, maybe it's 50%

but we really don't know how

long it lasts,

I think that's not a good risk

benefit calculus to give people,

and I think

that undermines vaccine


DR. JOHN WHYTE: But I think

the problem too is people

are misinterpreting the data.


DR. JOHN WHYTE: Some people are

saying it's 90% effective

after does one.

They're not taking those points

that you're considering.

I know Dr. Topol got

the vaccine.

I'm getting the vaccine

next week.

May I ask you gentlemen,

are you scheduled to get

the vaccine?

Have you gotten it already?

DR. STEPHEN HAHN: John, I have

not gotten it, and I'm waiting

for my provider to tell me when

it's appropriate for me

to get in line and get it.

But I can tell you, there's

no hesitation on my part.

When it's my turn,

I'm going to take the vaccine.

I do have an adult child who's

gotten it, because he's a health

care worker, and tolerated it

very well.


in the exact same position.

I'm lined up-- as soon as it

comes my turn, I'm there.

So it's just a matter of us

getting to-- those of us who are

essentially office workers,

we're a little lower on the list


DR. JOHN WHYTE: I want to ask

all of you, and including Dr.

Topol, because Dr. Topol,

you've been such

a great communicator

on your Twitter page.

So many of us let's turn there,


during the advisory panels

to see, what is Dr. Topol

talking about?

And I don't know how you always

have these great images

and charts and graphs.

I mean, I can't pull it


So having said that,

how do we interpret--

and let's be honest,

it's on everyone's mind--

these mutations in the strain?

DR. ERIC TOPOL: I'm really

glad you brought that up, John,

because I did

want to ask Steve and Peter

about this.

Because we have

this so-called B117 variant

in the UK and other countries,

but predominantly seen

in the UK.

It has 23 mutations.

There's a couple

in the spike protein which are

particularly incriminating.

And it's also one

of those mutations is shared

by a South African variant,

this so-called N501Y.

And what's interesting--

and I just posted a really deep

discussion about this

with one

of our guru structural


He talked

about the molecular high-five,

the two tyrosines and how this

could really make this virus

entry into the cell facilitated,

which is more transmission.

But what I wanted to ask Steve

and Peter was, OK, we're

going to probably see

further drift and evolution

of this virus.

We're already starting to see it

beyond the pandemic dominant

614, the D614G.

So there's going to be a need

for booster shots at some point,

whether it's at one year

or whenever.

Do we have to go through trials

at that point?

What's going to be your stance

regarding these adjustments

or tweaks on the vaccine to take

into account the drift

of the virus?

Because this virus unfortunately

is not going away.


Eric, I'm going to let Peter

answer that last question

from a regulatory point of view.

But just the other thing

that this is important for

is the diagnostic tests.



the variants--

are the test going to have

the same level of sensitivity

specificity predictive value

that they do now?

And it's something

that our teams at CDRH

are all over and are actually

looking at right now.

So, Peter, with respect

to vaccines.

DR. PETER MARKS: Yeah, no.

So great question on vaccines,

because I think we are,


this virus is starting to look

like it wants to become like Flu

Two, Son of Flu, or Father

of Flu,

with this kind of strain drift.

The nice thing about the flu

though, is it's set up for us

a very nice paradigm for strain

change supplements.

And so we will not need--

I think especially

with the mRNA-based vaccines,

I think we know how they work,


We will probably just have

to set up, essentially

what will be strain changes.

It might be the first time we do


we'll check

an immunogenicity study.

But it's not going to have to be

another 30,000 patient

clinical trial.

Those immunogenicity studies are

usually 400 patients, just

to make sure that we have

the right check of what's coming


And even that may not

be necessary after we check

at the first one or two times.

So I think we'll have a way

of evolving here with these.

And that brings to mind

that the three things that we

really need to know right

now that I'd love to know

is, do these vaccines stop

asymptomatic transmission,

how long will they give us


and what will be their spectrum,

in terms of dealing

with these various mutants that

seem to be coming up?

Which, uh.

You just--


DR. PETER MARKS: You just wonder

where it's going to go now.

It keeps me up at night.

DR. JOHN WHYTE: I got to ask

the first question.

I want to give Dr. Topol

the option to ask

the last question.

DR. ERIC TOPOL: I had two

quick questions for you

before wrapping up if I could.

One is, to just give us a word

about your view

on these rare, severe allergic


The word out there is it could

be the polyethylene glycol

or it could be the lipid


That's one question.

And the other one, if you

could just speak to--

this is that superhuman vaccine

immunity that is better

than the typical person,

that the concept

that you had 3% of people

in the Pfizer trial, 2.2%

in Moderna that turned out

that they were previously

infected with COVID.

And so the fact

that you had a readout now

of people who had

a prior infection, who

got placebo or got vaccine,

what does that tell us

about the vaccine-induced


versus the native intrinsic

infection response?

So if you could just give us

a little response on the allergy

and this concept of vaccine

versus natural infection


DR. PETER MARKS: This concept

of natural versus

vaccine-induced immunity--

I think the most important piece

for me that I'd draw from that

is that we're not seeing

this antibody

dependent enhancement.

If you got vaccinated

and it already had the virus,

we're not seeing

an adverse effect there.

And that's

consistent between both

of the vaccine trials, which

is reassuring to us.


DR. PETER MARKS: Because we


it would be very

cumbersome to screen people

for infection before vaccinating


I think the CDC has recommended

90 days, if you've actually had

COVID-19 before you go get



DR. JOHN WHYTE: Or received

monoclonal antibodies.





So I think that that makes


And so that's where I'll leave

it with that one because

of the time.

The allergic reactions--

something we are working very

closely with the Centers

for Disease Control

and Prevention

and with the companies

to make sure we keep very good

track of.

I know every day I get

an update.

This good news is, as we're

seeing them settle out,

I think it's not like the number

of them are increasing wildly.

I think we're going to see these

as events that are going to be

in the range, hazard a guess

of in the range of one in 50,000

something, one in 100,000.

But thankfully they have been

generally controllable

with typical measures

such as epinephrine and-or


We're going to have to keep

looking at them, and we're going

to try to delve into what

is causing them.

We will be looking into seeing

whether these could be-

could these these IgE antibodies

to polyethylene glycol?

We will look into that

and try to determine what we can

to try to help make

these vaccines as

safe as possible to use.


Thank you.

DR. JOHN WHYTE: Dr. Hahn, I want

to give you the final word.

DR. STEPHEN HAHN: Just really

appreciate being able to do


We're very concerned

and continue to work

on the issue of hesitancy

and confidence.

I'm incredibly proud of CBER

in the work that they did

and the transparency associated

with it,

and the 17,000 employees at FDA

who have just, again,

been heroic

throughout the pandemic.

So thanks for the opportunity

for us to join you today.

DR. ERIC TOPOL: Well, you've

really taken the FDA

in this time--

you've got to be so

proud of what you're

able to accomplish getting

these two over the goal line

so fast

and changing the whole way

that we get out of this mess,

which is a real mess.

So we're so grateful to you

and all the people you work

with to make this thing happen,

and in such an extraordinary way

and speed that we'll go back

to Peter's Project Warp Speed.

But it really paid off.

So we thank you both

and everyone.

DR. JOHN WHYTE: Let me echo that

on behalf of WebMD and Medscape.

You really have provided us now

the opportunity to crush

the pandemic, and vaccination is

that pathway to return

to normalcy.

So thank you both.

DR. PETER MARKS: Thank you so


DR. STEPHEN HAHN: Take care.

Thanks, John.

John Whyte, MD, MPH, Chief Medical Officer, WebMD. <br>Eric Topol, MD, Executive VP, Scripps Research, Editor-in-Chief, Medscape. <br>Stephen Hahn, MD, Commissioner of Food and Drugs, FDA. <br>Peter Marks, MD, PhD, Director, Center for Biologics Evaluation and Research, FDA./delivery/aws/0d/0d/0d0d1655-299e-3d4a-a3ce-33448fe359f9/Topol_Hahn_Marks_122320_v3_,4500k,2500k,1000k,750k,400k,.mp412/28/2020 15:43:0018001200Topol_Hahn_Marks_122320_1800x1200/webmd/consumer_assets/site_images/article_thumbnails/video/covid19-images/Topol_Hahn_Marks_122320_1800x1200.jpg091e9c5e820bed91

Viruses mutate often, and several variants of the coronavirus have been reported this year. Most mutations don’t have significant impacts on the spread of the disease. The U.K. variant appears to be more contagious, which could lead to a further spike in cases.

“If you have twice as many cases, then even if the amount of people who are sick is the same rate as it is currently, that would definitely be bad,” Diane Griffin, MD, an immunology professor at the Johns Hopkins Bloomberg School of Public Health, told NBC News.

The variant has been confirmed in more than a dozen countries, including Canada, France, Japan, and South Korea. Another variant has been identified in South Africa. Researchers in the U.K. have said the variant found there doesn’t seem to cause more severe COVID-19, though public health experts are concerned that the increase in transmission will lead to more hospitalizations and deaths.

“An increase in something that grows exponentially (i.e. transmission) can have far more effect than the same proportional increase in something that just scales an outcome (i.e. severity),” Adam Kucharski, PhD, an epidemiologist at the London School of Hygiene & Tropical Medicine, wrote on Twitter.

The variant has also been linked to higher loads of the virus in respiratory samples, according to a new U.K. study published on a preprint server on Sunday. Among 641 samples from COVID-19 patients who had symptoms, 35% who were infected by the variant had high viral loads, as compared with 10% who didn’t have the variant.

“It does seem as though the patients with this variant have higher viral loads -- then the obvious thing is it is easier for them to spread it to other people,” Michael Kidd, one of the study authors at the Public Health England laboratory in Birmingham, told The Guardian.

Now researchers are studying how the variant reaches a high viral load and how that plays a role in transmission.

“Like pieces in a jigsaw, we need other evidence,” Kidd said, adding that the study offers an “on-the-ground explanation of why this virus may have the ability to spread more easily -- because patients are more infectious.”

WebMD Health News Brief


NBC News: “Colorado reports first confirmed case of UK coronavirus variant.”

Twitter: @GovofCO, Dec. 29, 2020; @AdamJKucharski, Dec. 28, 2020.

CNN: “Colorado officials suspect they've found a second case of UK coronavirus variant.”

MedRxiv: “S-variant SARS-CoV-2 is associated with significantly higher viral loads in samples tested by ThermoFisher TaqPath RT-QPCR.”

The Guardian: “New Covid variant linked to higher viral load in respiratory samples.”

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