Jan. 29, 2021 -- An international team of researchers studying COVID-19 has made a startling and pivotal discovery: The virus appears to cause the body to make weapons to attack its own tissues.

The finding could unlock a number of COVID’s clinical mysteries. They include the puzzling collection of symptoms that can come with the infection; the persistence of symptoms in some people for months after they clear the virus, a phenomenon dubbed long COVID; and why some children and adults have a serious inflammatory syndrome, called MIS-C or MIS-A, after their infections.

“It suggests that the virus might be directly causing autoimmunity, which would be fascinating,” says lead study author Paul Utz, MD, who studies immunology and autoimmunity at Stanford University in Stanford, CA.

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COVID-19 Mutations Demand Immediate ActionWebMD's Chief Medical Officer, John Whyte, MD, speaks with Ashish K. Jha, MD, Dean, School of Public Health, Brown University, about immediate actions needed to confront the COVID-19 mutations. 667


DR. JOHN WHYTE: Welcome,


Thanks for tuning in.

I'm Dr. John Whyte, Chief

Medical Officer at WebMD.

And you're watching Coronavirus

in Context.

A lot of folks have questions

about these mutations,

these strands.

Should we be worried about it?

And how are people rating

the distribution plan

of the vaccine?

Is it a success?

And does it depend on where you


So to help provide

some insights, I've asked one

of the leading experts

on COVID-19, Dr. Ashish Jha.

He is the Dean of Brown

University School of Public


Dr. Jha, thanks for joining me.

DR. ASHISH JHA: Thank you

for having me here.

DR. JOHN WHYTE: Let's get right

to it.

People want to know

about these mutations, even

the words--

mutations strains.

How concerned should people be?


So let's just talk a little bit

about the words.

Mutations are pretty common.

Basically, every time the virus

replicates, there are

a few mutations here and there.

99.999% of them have no meaning.

They don't have

any clinical significance.

They're no big whoop, as they


The problem is, every once

in a while,

one of these mutations

becomes functionally important.

It becomes either more

contagious or more lethal

or, in some other ways,


And that's what's happened.

Now we have

a few different mutations that

have acquired

these functional differences

that means that they really are

different strains.

I think we've heard about them--

the UK variant,

the South Africa one, one

from Brazil, maybe one from LA,

though we're still sorting that


I've been hearing about strains

all through 2020.

And most of the times

I looked at the data

and shrugged my shoulders

and said, eh, there's not

much to see here.

DR. JOHN WHYTE: Does strain mean

it's a new virus?

Some people are saying,

is it new?

Is it different?

Does it matter?



Same virus.

Works in the same way, but just

a bit more contagious, or a lot

more contagious.

And here's what's going on.

On a molecular level, basically

the spike protein, those little

spikes on the virus--

that's what is really

important for attaching

to human cells

and infecting people.

There have been these mutations

on the spike protein that just

makes it attach more efficiently

and infect cells more


And that's bad, of course.

And so the UK variant really

does look like it is more


As opposed to all the mutations

of 2020

that I felt like we could blow

off, this one is not one we can

blow off.

This is a serious--

this is an important issue.

DR. JOHN WHYTE: So when it's

serious, what does that mean

for listeners?

Does that mean we definitely

need to try to speed up vaccine


Serious sounds serious.

So what should people do?

DR. ASHISH JHA: And I don't say

serious lightly.

It is serious because what we

are going to see

is we're going to see

this variant take off

across the country.

We're going to see it cause

large spikes in infections

and hospitalizations and deaths.

And we got to do everything

we can to prevent it.

So what do we need to do?

We absolutely need to be

vaccinating many, many more

people as quickly as possible.

Probably our single most

powerful tool in the short run.

Probably all of us

need to be upgrading our masks

and the masks

that we're wearing.

I think the standard cloth masks

we've worn through 2020--

probably not good enough

for this variant.

We need better quality masks.

DR. JOHN WHYTE: Do we need

a double mask?

DR. ASHISH JHA: A double mask

can be pretty


under certain high-risk


So if you're out for a walk

with your dog, you probably

don't need a double mask.

Even a simple cloth mask

is maybe OK.

But if you're going to go

into a room with a bunch

of other people, I think double

masks, certainly high-quality

masks like KN95s or KF94s--

these are all

available on Amazon

and other retail stores.

Those are generally higher

quality masks.

A good surgical mask is also

quite useful.

But again,

in high-risk situations,

a double mask may be the thing

that's needed.

DR. JOHN WHYTE: What about

the multi-layer cloth masks

that maybe you put a filter in,

a coffee filter?


I think a multi-layer cloth mask

with a filter can be quite good.

It really depends there on fit,

if you have a really good fit,

a good seal.

Again, you got to cover

your nose.

It's got to come

below your chin.

I think that can also be quite


DR. JOHN WHYTE: You're a dean,

so you're used to giving grades.

So I want you to grade

the distribution of COVID-19's


Would you give it a gentleman's


Would you give it an F?

Is it a D?

What grade is it?

DR. ASHISH JHA: Well, it's

certainly not an A or a B.

So I would probably say it's

somewhere like a C minus,

D plus.

DR. JOHN WHYTE: Was there even

a plan, Dr. Jha?

Some people are saying,

there wasn't actually even

a plan.

It was just, let the states do


And here they did a great job

in terms of development

of vaccines.

And then when it comes time

to get it out, some people could

argue it's worse

than the testing debacles

that we've had.

Why so wrong?

How do we fix this?


So it has been a debacle.

I think debacle is a good word

for it.

Basically, there was not

much of a federal plan.

The people who put this together

on part

of the federal government,

fundamentally just misunderstood

vaccinations and how it works.

They just said, well, we'll let

states figure it out.

Everybody will go to their CVS

and get it.

Didn't think through the details

and certainly didn't have

any sense of urgency

and then made a whole bunch

of predictions like 20 million

will be vaccinated by December,

50 by January, that clearly was

never going to come true.

So a lot of disappointment

and frustration.

But I think if we look forward,

the way I see it is states

are starting to figure this out.

The new federal government has

been very clear that they're

going to work with states

to augment state capability.

I do think we can turn this


But it's going to take

a lot of work

and a lot of resources.

DR. JOHN WHYTE: When do we need

to turn it around?

Do we have several week leeway?

There are several states where

people are having

the second shot appointment


And my concern

is that some people are just

going to say, well, I got one.

That's better than none.

And that's not necessarily true.

So how much leeway do we have?

And does all of this decrease

confidence in vaccination--

we're making some progress

in terms of people

willing to take the vaccine.

And now people can't even get it

or can't get their second shot.

So it becomes, why bother?



So a couple of things.

First, when do we need to turn

this around?

Yesterday would be a good day

to have turned this around,

meaning that we don't have time

to lose on his.

And the second point

is, absolutely everybody needs

a second vaccine.

If you've gotten one shot

and you're wondering,

do I need a second-- yes,

you do.

You need that second shot

because that's what's going

to give you

a durable protection.

One shot will give you

inadequate protection that will

wain over time.

So in my mind,

it's a no-brainer.

Everybody needs to get

a second shot.

Look, the new team has a lot

of work to do.

They just got into office.

They've got to sort out

the details.

I think we've got to give them

at least a few days to come up

with a plan.

The plan they have so far

looks good, but it's going to be

the reality on the ground of,

how many vaccines do we have?

What are the capabilities

of the states and how do we

augment it?

If people have had

their second doses canceled,

they need to get rescheduled

more or less right away.

And we've got to get

the vaccines out to individuals.

So there's a lot of work to do.

I remain pretty optimistic we

can do it, but there is going

to be a lot of work.


And the President has talked

about 100 million shots in 100


So that's a million shots a day.

We're at about 800,000-900,000.

But some experts, as you may

know, Dr. Jha, have been

arguing, we need to be at 1.4


if we want to vaccinate everyone

by the end of summer.

How optimistic are you

that we're going to be

able to get to--

we need to be at more

than a million

because we need to make up

in terms of what's going on.

And then we need people

to actually sign up.

And that's where the frustration



So I'm pretty confident.

We're going to get there.

Here's why.

Look, the first couple of weeks

of the administration

is going to be tough.

They're going to be picking up

the mantle.

They're going to be trying to do

a lot of stuff.

And I wouldn't be surprised

if they can't quite hit

a million a day.

But I think over time you are

going to see more.

There are a couple of things

that give me optimism.

Right now we have Moderna

and Pfizer.

I'm hoping we'll have Johnson

& Johnson online soon.

We may have Novavax.

We may have AstraZeneca.

So these are, again--

we don't know.

We don't know.

And I don't want to count

on those.

DR. JOHN WHYTE: Those are

expected not to have

good manufacturing capabilities

until April.

So even if they apply for EUA

in February, that's a couple

of months away.

To your point,

if we have this variant that's

more transmissible,

we need to be getting shots

in the arm now.

DR. ASHISH JHA: Absolutely.


And I don't think any of them

are going to make a material

difference, as you said,

until April.

We may see some impact, maybe

of J&J, by March.

But again, not a lot of doses.

So right now, between now

and March, it's largely

a Moderna and Pfizer game.

But once we get into April,

we could have help

from several other vaccines.

And that's why I do think

within 100-day target--

we're going to hit that.

But the question is, how much

of that can we do front loaded?

And that's where the game

of trying to outpace the variant

is all about.

100 days is too

late for the variant.

We've got to move in the next 30

to 60 days.

DR. JOHN WHYTE: And finally, I

want to ask you

about public health.

Here you're at one of the most

prestigious schools.

You're working with students who

are excited about being involved

in public health.

Do you think the way the public

perceives public health is

changed because of COVID?

And has it changed

for the better?

Because in some ways,

people may be saying,

you know what?

Hasn't worked out so well.


I think a majority of Americans

are pretty-- well, first of all,

I should actually start off

by saying, I think most people

didn't even know what

public health was.

I think people now know what

public health is.

DR. JOHN WHYTE: They think it's

the water supply.



So people now know what

public health is.

You don't have to explain it

to folks.

I think the second is, most

people have seen

the public health community

as part of the solution,

that they've been helpful.

And we haven't gotten everything


There have been missteps.

But in general, I think people

have relatively favorable views

of public health.

I'll tell you.

At our school,

we've seen a greater than 100%

increase in our applications.


DR. ASHISH JHA: There is so much

interest in public health

right now, just

excitement about people

who want to come and learn

public health

and study public health

and do public health.

And I think that's great.

And we've got to turn

that excitement into education

and learning and action.

So I'm pretty

optimistic about the future

of public health.

I wish it didn't take

a horrible crisis like this just

to stir it on.

But if that's one

of the silver linings, that's

OK, I guess.

DR. JOHN WHYTE: Well, we'll

leave it at that.

Dr. Jha, I want to thank you

for taking the time today

and sharing your insights.

DR. ASHISH JHA: Dr. Whyte,

thank you for having me on.

I really appreciate it.


John Whyte, MD, MPH, Chief Medical Officer, WebMD.<br>Ashish K. Jha, MD, Dean, School of Public Health, Brown University./delivery/aws/dd/ed/dded31f6-75cc-3955-83df-b2ec27f5f199/Jha_012121_v3_,4500k,2500k,1000k,750k,400k,.mp401/25/2021 12:00:0018001200Jha_012121_1800x1200/webmd/consumer_assets/site_images/article_thumbnails/video/covid19-images/Jha_012121_1800x1200.jpg091e9c5e820ece89

The study, which has not yet been peer reviewed, also deepens the question of whether other respiratory viruses might also break the body’s tolerance to itself, setting people up for autoimmune diseases like multiple sclerosis, rheumatoid arthritis, and lupus later in life.

Utz says he and his team are next going to study flu patients to see if that virus might also cause this phenomenon.

“My prediction is that it isn’t going to be specific just to SARS-CoV-2. I’m willing to bet that we will find this with other respiratory viruses,” he says.

The study comes on the heels of a handful of smaller, detailed investigations that have come to similar conclusions.

The study included data from more than 300 patients from four hospitals: two in California, one in Pennsylvania, and another in Germany.

Researchers used blood tests to study their immune responses as their infections progressed. Researchers looked for autoantibodies -- weapons of the immune system that go rogue and launch an attack against the body’s own tissues. They compared these autoantibodies to those found in people who were not infected with the virus that causes COVID.

As previous studies have found, autoantibodies were more common after COVID -- 50% of people hospitalized for their infections had autoantibodies, compared to less than 15% of those who were healthy and uninfected.

Some people with autoantibodies had little change in them as their infections progressed. That suggests the autoantibodies were there to begin with, possibly allowing the infection to burn out of control in the body.

“Their body is set up to get bad COVID, and it’s probably caused by the autoantibodies,” Utz says.

But in others, about 20% of people who had them, the autoantibodies became more common as the infection progressed, suggesting they were directly related to the viral infection, instead of being a preexisting condition.

Some of these were antibodies that attack key components of the immune system’s weapons against the virus, like interferon. Interferons are proteins that help infected cells call for reinforcements and can also interfere with a virus’s ability to copy itself. Taking them out is a powerful evasive tactic, and previous studies have shown that people who are born with genes that cause them to have lower interferon function, or who make autoantibodies against these proteins, appear to be at higher risk for life-threatening COVID infections.

“It seems to give the virus a powerful advantage,” says study author, John Wherry, PhD, who directs the Institute for Immunology at the University of Pennsylvania.

“Now your immune system, instead of having a tiny little hill to climb, is staring at Mount Everest. That really is devious.”

In addition to those that sabotage the immune system, some people in the study had autoantibodies against muscles and connective tissues that are seen in some rare disorders.

Utz says they started the study after seeing COVID patients with strange collections of symptoms that looked more like autoimmune diseases than viral infections -- skin rashes, joint pain, fatigue, aching muscles, brain swelling, dry eyes, blood that clots easily, and inflamed blood vessels.

“One thing that’s very important to note is that we don’t know if these patients are going to go on to develop autoimmune disease,” Utz says. “I think we’ll be able to answer that question in the next 6 to 12 months as we follow the long haulers and study their samples.”

Donna Farber, PhD, a professor of microbiology & immunology at Columbia University called the study's findings very interesting. She points out that most of the patients in the study appeared to be extremely ill and suffering from extensive organ damage from their infections.  She says one possible explanation for the autoantibodies could be that the body is producing them to try to check it's own raging immune responses to the virus.

"Rather than driving the disease, these antibodies are formed in response to the high level of tissue and inflammatory molecules released due to the virus-associated and immune mediated damage," she says. "Many types of infections can lead to transient autoimmunity or autoimmune disease--that is well established," she says.

 Farber, who was not involved in the study, says long covid seem to be uncommon and for those affected, eventually goes away.  All this suggests that "this virus can really hit the body, but doesn’t alter the immune system to lead to long-term autoimmune disease."

Utz says it will be important to study autoantibodies in long haulers to see if they can identify exactly which ones seem to be at work in the condition. If you can catch them early, it might be possible to treat those at risk for enduring symptoms with drugs that suppress the immune system.

And more study will be needed to find out whether this autoimmune attack persists. One thing is for sure, he says: COVID will be with us for a long, long time.

“We have to realize that there’s going to be long-term damage from this virus for the survivors. Not just the long haulers, but all the people who have lung damage and heart damage and everything else. We’re going to be studying this virus and it’s badness for decades,” Utz says.

WebMD Health News


BioRxiv, Jan. 29, 2021.

Paul Utz, MD, professor, immunology and rheumatology, Stanford University, Stanford, CA.

John Wherry, PhD, chair, Department of Systems Pharmacology and Translational Therapeutics, University of Pennsylvania, Philadelphia.

Donna Farber, PhD, professor, Microbiology & Immunology, Columbia University, New York, New York

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