Translating a Recent Scientific Discovery about Covid19

well hello everybody who’s

listening uh virtually um my name is

bruce patterson

and i’m a virologist uh you probably

haven’t heard of virologists

in the past but all of a sudden now

i think we’re in the middle of an era

where we we need

uh virologists you’re going to see me

smile

and be relatively hopeful because i am

hopeful

the other thing is we’ve already saved

lives with the approach

that i’m going to talk about and we’re

hoping to save even more lives

as we go through fda clinical trials

with an exciting new drug

that we developed based on

a discovery that i’ll talk about

shortly now everybody’s heard about

kovid

there’s so much information out in the

media

and in the world about how it works and

how infectious it is and

i hope to at least address some of those

issues

i came back from china in january

talking to a company over there about

doing a deal when i first heard about

this virus

that that was emerging

and it brings up a very interesting word

that we’re hearing a lot about which is

emerging infections and what does

emerging infections mean

it means they’re infections that our

bodies haven’t

seen before so that’s a very interesting

conundrum for the human body because

we basically have a storage vault

of immune responses against pathogens

bugs bacteria viruses

uh parasites that the body uses

when you’re infected with those uh with

those

particular pathogens again emerging

infections are something that our body

has never seen before

but the body actually has some very

elegant ways

uh rudimentary ways although

that to fight off these emerging

infections

and that’s part of what i’m going to

talk about because that’s part of what

happens

uh in covid okay so where do we do all

this work well

my company in cell dx specializes

in developing novel approaches to both

diagnosing

uh particular pathogens looking at how

the pathogens work

uh working with companies that have

therapeutics

that can potentially work for these

pathogens

and then most importantly using the

diagnostics to say that the

therapeutic is actually working so

we’ve all heard about the different

diagnostics and the shortage of

diagnostics

that are out there uh in the world and

those really revolve around

do you have the virus yes or no that was

the first wave of diagnostics

the second wave of diagnostics was have

you been exposed to the virus

and do you have immunity to the virus

now those are two

very different questions but the third

level of diagnostics that we started

thinking about over two months ago

was how can we design diagnostics and

laboratory tests that say whatever we

try on a patient is actually working

and that’s the whole area of

personalized medicine that we’re in

these days

and usually we apply that to cancer but

the fact is personalized medicine can

also be applied

uh to infectious disease and that keeps

patients from having to take every

one drug or another drug and act as a

guinea pig until one of them works

we want to know before you get a drug

when it’s going to work

how it’s going to work when do you give

it and how much do you give

and most importantly is the drug safe

so we hear a lot about the drugs are out

in the market about covid

and the fact is the big question are

they really safe

do they cause kidney problems they cause

liver problems

are they immunosuppressive like the big

dexamethasone that we’ve heard over the

last few days which is

basically a steroid that completely

immunosuppresses

individuals who are already

immunosuppressed

well i’ll digress back to covet and the

whole covid

story right now when we first

looked at covid it was very interesting

because we saw

patients who look very much like aids

patients

aids patients have low quote cd4

lymphocytes which is part of the immune

system against viruses

the other cell that’s involved in the

immune system against viruses is called

a

cd8 t cell whereas aids has

low cd4 counts covate has very low cd8

counts

but the the but at the end of the day

they create the same situation

that is immunosuppression so what do we

see in covid patients

well it’s very interesting i’ll skip

forward a couple of slides

we now know that covid goes in about two

different phases there’s an initial

phase which we call the virologic phase

you’re infected you have a positive

covid test

maybe you feel okay but the virus is in

your body

and it’s replicating maybe it progresses

maybe it doesn’t that’s one of the

biggest questions

and i would say that one of the biggest

concerns about kovid

is that it’s unpredictable you know this

is my

fourth pandemic i

started my career in hiv

which developed a lot of the tools that

we’re using today

in covid and then i was a head of

virology at stanford during

sars one and the h1n1

flew in the late late 2000s

and there are very similar themes

in all of these pandemics however

kovid is one that has been highly highly

unpredictable

it starts out as a viral disease but at

some tipping point which you see in the

middle of this slide

it goes from being a virologic disease

to an

immunologic disease and it’s the

immunologic disease

in its severest form that causes the

damage of the lungs

the damage to the kidneys the damage to

the liver the coagulation that you see

with strokes

amputations that were seen recently and

even

in kids a disease that’s similar to

what’s called

kawasaki’s disease which is basically

extreme

inflammation of blood vessels including

the coronary arteries

that can cause death in some of these

kids

as i’m saying this you can see how

unpredictable and unusual this viral

infection is in terms of all the

different manifestations that it causes

well what is this switch in the middle

of this slide

that causes covid to go from a virologic

disease

to an immunologic disease now that was a

big question two and a half months ago

when i was working with my chinese

colleagues

and trying to figure out what was

happening we were in the middle of

developing some tests for them

we looked at what was called cytokines

cytokines are proteins that are made by

immune cells

and other cells to basically confer

function on your body’s immune system

for the most part and cytokines are

involved in

moving cells around your body to fight

off these different pathogens no matter

where they are

so it’s a very interesting set of

proteins that get released

into the circulation and we found very

high levels of this one protein called

rantes

or ccl5 in all of these patients across

the board

in covet infection why is that important

well rantes is like a magnet

when rantis is produced it pulls immune

system

immune cells from all over your body

into these areas of inflammation

right now that’s fine that’s what it’s

supposed to do

except when it’s overactive and

unlike some of the other proteins that

make up what’s called the cytokine storm

which is

what everybody’s hearing about on cnn

and other shows which is just this

mass release of these proteins that are

supposed to confer

immune functions but it’s it’s

overzealous

it’s hyper immunity and it’s actually

causing lung damage and kidney damage

and liver damage

and coagulation that’s a problem

but it’s all being driven by the fact

that this one protein rantes

is pulling in the cells that make these

proteins that make up the cytokine storm

so what does that mean for us in terms

of therapies

and for vaccines for that matter well

the fact is

with emerging infections we don’t have

any tools any drugs any vaccines

that are specific for the emerging

pathogen and that’s a big shortcoming in

terms of the world and how we prepare

for the next pandemic we need to have a

stockpile of drugs

that have a general broad

application against pathogens that we

may not even know about

because it’s going to take 12 to 18

months to come up with pathogen-specific

therapies or vaccines for that matter

and so you know what can we do about

that well

what we’ve learned in cancer over the

past five years

is the most powerful drug against

cancer is our own immune system

we found drugs like optivo and katruda

and some of these others

that bring back the immune response

against tumors okay there was a case

when i was working with a large

pharmaceutical company

where there was a melanoma the size of a

golf ball

they took 12 months of one of these

quote immuno oncology drugs

that restored the immune response and by

the end of 12 months it was the size of

a freckle

and you could scrape it off with a

scalpel blade

now my original thinking back two and a

half months ago when we had this

emerging infection is

let’s manipulate the immune response

like we’re manipulating the immune

response in cancer

let’s do that to this virus

and see what happens and in fact

when we found this rantes there was a

great drug called larondemab

that actually blocks the binding of this

rantes to immune cells

and actually prevents this mass

migration of cells

into non-specifically into the lung and

other organs

and relieves uh and quiets

this storm of bad proteins that are

causing all the the immune damage in

these patients

and in addition it restored the

immunosuppression so these patients were

horribly immunosuppressed

they took the drug and their their

levels of their lymphocytes their cd8

cells went back to normal

then surprisingly unlike this drug wren

desevere which was just approved which

is the antiviral

this drug laron lamab actually dropped

the amount of virus it shut off the

viral replication

and by 14 days the viral burden

was zero okay

now the biggest question when this rem

deserver got approved was

why is this antiviral not shoving off

virus

and that’s what led me to be skeptical

about that as a therapy

because the three things you need in

covid are

a quiet this so-called cytokine storm to

prevent all the lung damage and

organ damage b restore the immune

response because these patients are

immunosuppressed and could die of

bacterial infections

or other viral infections and c

stop the virus now

the government fauci and others have

proposed well that may take

two drugs well what’s fascinating about

our study that we

we we just published uh in the pre-print

journal

uh was that this drug laurentlamab did

all three of those it quieted the

cytokine storm

it restored immunosuppression and it

dropped the virus

what more than you need in in covid

so the goal for covid therapy

is really to address these phases of

disease

and like i said it’s very very

unpredictable

we don’t know which patients are going

from this virologic phase

to the immunologic phase there’s not a

marker although we think

rantis may be that marker the the

protein that we discovered

at ncdx and the fact is this drug

laurentlamab

in early phases may prevent the

transition from

virologic or mild disease to severe

disease

and in late disease would reverse all of

these changes

in immunosuppression that i just

mentioned

and the fact that i’m smiling or at

least

glowing a little bit is the fact that

this drug has saved lives

at the end of the day we have already

saved lives

would we love to save more absolutely

we’re in the middle of two

big uh fda clinical trials one for mild

to moderate disease

one for severe disease and if it turns

out how we

expect and again we’ve seen data on

hundreds of patients

over multiple multiple weeks of therapy

we’re hopeful and we’re excited about

the possibility

that this drug can keep patients from

going from mild disease to severe

disease

and in the severest of diseases

save lives and and that is

the goal of all covid therapy and that

is a therapeutic

now everyone’s talking about the

vaccines and how quickly they’re they’re

coming out

big lesson from hiv okay we used to hear

reports about

successful trials of vaccines

yeah phase one they were safe you could

give the vaccine and they wouldn’t get

hiv

right so the two biggest hurdles in

vaccines

are does it make antibodies

that help fight off infection

and are those antibodies effective those

are the two big hurdles that remain

for for vaccines this virus mutates

uh and has high sequence variability

around the world

so you know it’s it’s not quite as

mutating as uh as hiv but you know

that gives me pause as well about the

ultimate efficacy of vaccines

but i’m very hopeful that we have

therapeutics

and if we have therapeutics that prevent

death

and therapeutics that prevent morbidity

i we can get back to work this becomes

just another

viral infection like the influenza

or or other respiratory viruses that we

get in the winter

because it’s something that we can deal

with and we can prevent the death

the problem was in covid which is also

worrisome with

with the relaxation of all these um

shelter in place and of course we’ve

seen a massive

increase in cases due to that

my concern is people talk about

infection rates

and they talk about death rates and they

say the death rate is

relatively low relative to ebola and

maybe some other viruses

however nobody talks about the morbidity

in this disease this is not about do i

live or do i die

in the people who died relatively small

percentage

the problem is these people who get

infected

and have severe infection are not

better if you look at this graph

it goes out to 30 days 30

days after infection some people

have not gotten back to normal when we

get the flu

we get other respiratory viruses in the

winter we stay in bed for a week

we we we get our strength back a little

we go back to work the next week we’re

still a little weak maybe a little tired

but

at the end of two weeks you’re back in

the gym and you’re feeling fine

that is not the case in covid and we’re

not talking about it

these people are 30 days out 40 days out

their their their cytokines all their

blood work that i’ve been working with

in

hundreds and hundreds of patients over

time

30 days 40 days it’s not

normal it’s not back to normal and all

this inflammation

is making them not feel well

and there is the possibility that this

inflammation is doing damage

rantes this protein that we discovered

that i’m talking about

uh has been implicated in renal failure

has been implicated in liver you know

liver toxicity

has been implicated in coagulopathies or

coagulation

which is strokes and clots and all the

things you’re hearing about

these people who have to have

amputations

it’s all being driven by massive massive

amounts of inflammation and the hope is

drugs like laura momab will be able to

to be able to treat that but we have to

treat that for a long period of time

potentially

and rantes is a marker to tell us when

do you start treating because when do

you do

make that switch from a viral disease to

an immunologic disease

and how long do you treat but that’s

what our ability is in medicine right

now

is to give a drug and know what it’s

doing

we no longer use patients as guinea pigs

and let’s give this a try

let’s give that a try we know when to

start a therapy we know when to stop a

therapy

and ultimately that not only saves the

patient

pain and suffering but also saves health

care dollars

and i think some of the other talks

today are going to be the health care

and the economic implications of covid

which we also have to take into account

as we’re

moving forward uh with some of these uh

approaches but again i’m very hopeful

and i’m hopeful that we have a drug that

we have a therapy

that will remove the specter of death

remove the specter of horrible

morbidities

and makes this just another infection

and we can go about our business get

back to work

and get this economy restored

thank you i really appreciate the tedx

folks for inviting me it’s been very

exciting to do this

in my home uh country up here in

northern michigan and uh

be safe be well we’re working on it

thank you very much

好吧,大家好,几乎所有在

听的人,嗯,我的名字是

布鲁斯·帕特森

,我是一名病毒学家,呃,你过去可能

没有听说过

病毒学家,但突然之间,

我认为我们正处于一个时代的中间

,我们 我们需要

病毒学家,你会看到我

微笑

并相对充满希望,因为我

充满

希望另一件事是我们已经

我将要谈论的方法挽救了生命,我们

希望能挽救更多生命

当我们

使用一种令人兴奋的新药进行 fda 临床试验时,我们开发了一种令人兴奋的新药

,我很快就会谈到

现在每个人都听说过

kovid

媒体

和世界上有很多关于它如何工作以及

如何工作的信息 它具有传染性,

我希望至少能解决一些

问题

d 我们听到很多关于哪些是

新发感染以及

新发

感染意味着什么这意味着它们是我们的

身体以前从未

见过的感染所以这对人体来说是一个非常有趣的

难题,因为

我们基本上有一个存储库

对病原体的免疫反应

虫子 细菌 病毒

呃 寄生虫

当你感染那些 呃

那些

特定的病原体 再次出现的

感染是我们的身体

以前从未见过的东西,

但身体实际上有一些非常

优雅的方式

呃 基本的方式 虽然

这是为了对抗这些新出现的

感染

,这是我要

谈论的内容的一部分,因为这是在 covid 中发生的事情的一部分,

好吧,所以我们在哪里可以很好地完成所有

这些工作,

我在 cell dx 的公司

专门开发新的方法 诊断

呃 特定的病原体 看看病原体是如何

工作的

呃 与拥有

有效疗法的公司合作 通常为这些病原体工作

,然后最重要的是使用

诊断方法来说明

治疗方法确实有效,所以

我们都听说过不同的

诊断方法以及世界上存在的诊断方法的短缺,

那些真正围绕着

你 是否有病毒,是或否,这

是第一波

诊断第二波诊断是

你是否接触过病毒

,你现在对病毒有免疫力吗?

这是两个

非常不同的问题,但

我们开始的第三级诊断

两个多月前思考的

是,我们如何设计诊断和

实验室测试来说明我们对患者所做的任何

尝试实际上都在起作用

,这

就是我们现在所处的个性化医疗的整个领域

,通常我们将其应用于癌症,

但是 事实上,个性化医疗

也可以

应用于传染病,这使

患者不必服用每

一种药物或另一种药物 d 充当

豚鼠,直到其中一个起作用

我们想在您服用药物之前

知道它什么时候起作用

听到很多关于

市场上关于covid的药物的信息

,事实是最大的问题是

它们真的安全

吗?它们会导致肾脏问题吗?它们会导致肝脏问题吗?

它们是否像我们过去几天听到的大地塞米松一样具有免疫抑制作用

基本上是一种类固醇,可以完全

免疫抑制

已经

免疫抑制

良好的个体。当我们第一次看到 covid 时,我将回到 covid 和

整个 covid

故事

,这非常有趣,

因为我们看到的

患者看起来非常像艾滋病

患者

艾滋病 患者的 cd4 淋巴细胞报价低

,它是针对病毒的免疫系统的一部分,

而参与

针对病毒的免疫系统的其他细胞称为

cd8 t 细胞。 eas

AIDS 的 cd4 计数低 covate 的 cd8 计数非常低

,但是最终

它们会造成相同的情况

,即免疫抑制,所以我们

在 covid 患者中看到了什么,

这非常有趣,我将

跳过几个 幻灯片

我们现在知道新冠病毒大约有两个

不同的阶段 有一个初始

阶段,我们称之为病毒学阶段

你被感染了 你的新

病毒检测呈阳性 也许你感觉还好,但病毒在

你的身体里

,它正在复制,也许它会进展

这不是

最大的问题之一

,我想说的是,对 kovid 最大的

担忧之一

是它是不可预测的,你知道这

是我的

第四次大流行,我

开始了我的 HIV 职业生涯,

它开发了很多

我们正在使用的工具 今天

在 covid 中使用,然后我在 sars 一期间担任斯坦福病毒学负责

人,h1n1

在 2000 年代后期飞行

,所有这些流行病都有非常相似的

主题,但

kovid 是其中之一 它是高度

不可预测的,

它最初是一种病毒性疾病,但

在这张幻灯片中间的某个临界点,

它从病毒学疾病

变成

了免疫疾病,它是最严重的

免疫疾病

,导致

肺部损伤 肾脏

损伤 肝脏损伤 中风时出现的凝血现象

最近甚至在儿童中出现的截肢

一种类似于

所谓的

川崎病的疾病,基本上

是血管的极端炎症,

包括冠状动脉 正如我所说的那样

,可能导致其中一些孩子死亡的动脉

你可以看到

这种病毒感染是多么不可预测和不寻常

,就它引起的所有不同表现而言

,这张幻灯片中间的这个开关是

什么导致的 covid 从病毒学

疾病

转变为免疫学疾病现在这是

两个半月前的一个大问题,

当时我 正在和我的中国

同事一起工作

,试图弄清楚发生了什么

我们正在

为他们开发一些测试

我们研究了所谓的细胞

因子 细胞因子是由

免疫细胞

和其他细胞制造的蛋白质,基本上赋予

你的功能 身体的大部分免疫系统

和细胞因子都

参与了在

你身体周围移动细胞以

抵抗这些不同的病原体,无论

它们在哪里,

所以这是一组非常有趣的

蛋白质,它们被释放

到循环中,我们发现

这种蛋白质含量非常高

在所有这些渴望感染的患者中,一种称为rantes或ccl5的蛋白质

为什么重要

,rantes在产生rantis时就像磁铁一样,它会将免疫

系统的

免疫细胞从你全身

拉到这些

炎症区域 很好,这就是它

应该做的,

除非它过度活跃并且

不像其他一些蛋白质,它

构成了什么 被称为细胞因子风暴

,这

是每个人在 cnn

和其他节目中听到的,这就是

这些蛋白质的大规模释放,这些蛋白质

本应赋予

免疫功能,但它

过于狂热,

它是超免疫,它实际上会

导致肺损伤和肾损伤

, 肝损伤

和凝血是一个问题,

但这一切都是由这样一个事实驱动的,

即这种蛋白质

正在拉动制造这些蛋白质的细胞,这些

蛋白质构成了细胞因子风暴,

那么这对我们的治疗和疫苗来说意味着什么?

事实是,

对于新出现的感染,我们没有

任何工具 任何药物 任何

针对新出现的病原体的疫苗,这对于

世界和我们如何

为下一次大流行做准备来说是一个很大的缺陷,我们需要有一个

对我们

甚至可能不知道的病原体具有普遍广泛应用的药物储备,

因为这需要 12 到 18

个月才能实现 找出病原体特异性

疗法或疫苗

,这样你就知道我们能做些

什么了 我们在过去五年里在癌症方面学到的东西

是最强大的

抗癌药物是我们自己的免疫系统

我们发现了药物 像 optivo 和 katruda

以及其中一些

可以恢复针对肿瘤的免疫反应的其他

药物

引用

恢复免疫反应的免疫肿瘤药物,

到 12 个月结束时,它

有雀斑那么大

,你可以用手术刀刮掉它

现在我最初的想法是两个

半月前,当我们有这种

新出现的感染时 是

让我们操纵免疫反应,

就像我们操纵癌症中的免疫反应一样

让我们对这种病毒这样做

,看看会发生什么,事实上,

当我们发现这种咆哮时,有抗原

治疗一种叫做larondemab的药物

,它实际上阻止了这种

病毒与免疫细胞的结合

,实际上阻止了这种

细胞大规模迁移

到非特异性地进入肺和

其他器官,

并缓解了呃和平息

了导致所有免疫的坏蛋白风暴

这些患者的损伤

,此外它恢复了

免疫抑制,因此这些患者受到了

可怕的免疫抑制,

他们服用了这种药物,他们

的淋巴细胞水平,他们的 cd8

细胞恢复正常,

然后令人惊讶地不像这种药物 wren

desevere,它刚刚被批准,它

是抗病毒药物

这种药物 laron laab 实际上降低

了病毒的数量,它关闭了

病毒复制

,到 14 天,病毒

负担为零,

好吧,当这个

rem 应得者获得批准时,最大的问题是

为什么这种抗病毒药物不能驱除

病毒

,这就是导致我的原因 对此

作为一种疗法持怀疑态度,

因为您在新冠病毒中需要的三

件事是 即这种所谓的细胞因子风暴,以

防止所有肺损伤和

器官损伤 b 恢复免疫

反应,因为这些患者受到

免疫抑制,可能死于

细菌感染

或其他病毒感染,并且 c

现在政府 fauci 和其他人

提出了很好的建议 这可能需要

两种药物

我们刚刚在预印本期刊上发表的研究的

迷人之处 比你在covid中需要的多,

所以covid治疗的目标

实际上是解决这些疾病阶段

,就像我说的那样,这是非常

不可预测的,

我们不知道哪些患者正在

从病毒学阶段

进入免疫学阶段,虽然没有

标记 我们认为

rantis可能是我们在ncdx发现的蛋白质的标志物

,事实是这种药物

laurentlamab

处于早期阶段 s 可能会阻止

病毒学或轻度疾病向严重疾病的转变,

并且在疾病晚期会逆转

我刚才提到的所有这些免疫抑制变化,

而我正在微笑或至少

有点发光的事实是

这种药物的事实 最终拯救了生命

我们已经

拯救了

生命 我们是否愿意更绝对地拯救

我们正处于两个

大型 uh fda 临床试验中,一项针对轻度

至中度疾病,

一项针对重度

疾病 我们

期待并且我们再次看到了

数百名患者

在数周的治疗中的数据,

我们充满希望,我们对

这种药物可以防止患者

从轻度疾病转变为严重疾病

以及在最严重的疾病中的可能性感到兴奋 疾病可以

挽救生命,这

是所有新冠病毒治疗的目标,这

是一种治疗方法

过去常常听到

关于

疫苗成功试验的报道,

是的,第一阶段它们是安全的,你

可以接种疫苗,但它们不会感染

艾滋病毒,

所以疫苗的两个最大障碍

是它是否会

产生有助于抵抗感染的抗体,

以及这些抗体是否有效 这些

是疫苗仍然存在的两大障碍,

这种病毒会发生变异,

并且在世界范围内具有很高的序列变异性

所以你知道它

不像艾滋病毒那样变异,但你知道

这也让我暂停了疫苗的

最终功效。 疫苗,

但我非常希望我们有

治疗方法

,如果我们有预防

死亡

的治疗方法和预防发病的治疗方法,

我们可以重新开始工作,这

只是另一种

病毒感染,如流感

或我们进入的其他呼吸道病毒

冬天,

因为这是我们可以处理的事情

,我们可以防止

问题出现在 covid 中,这也

令人担忧

放宽所有这些

庇护所,当然我们

看到

病例大量增加,因为

我担心人们谈论

感染率

,他们谈论死亡率,他们

说死亡率

相对于埃博拉病毒和

也许其他一些病毒

但是没有人谈论

这种疾病的发病率这不是关于我

在死亡人数相对较少的人中是生还是死

在这张图中,

它持续到感染后 30 天 30

天 有些人

在我们感染流感时还没有恢复正常

我们在冬天感染了其他呼吸道病毒

我们在床上躺了一个星期

我们我们的体力恢复了一点

我们下周回去工作,我们

仍然有点虚弱,也许有点累,

在两周结束时,你回到

了健身房,你感觉很好

,这在 covid 中并非如此,我们

不说话 g 关于这件事

这些人 30 天 40 天

他们的细胞因子

我一直在与数百名患者一起工作的所有血液检查

30 天 40 天 这不

正常 它没有恢复正常等等

炎症使他们感觉不舒服,

并且这种

炎症可能正在造成损害

,我们发现我正在谈论的这种蛋白质,

呃,与肾功能

衰竭有关,与肝脏有关,你知道与

毒性有关 凝血病或

凝血

,即中风和血栓,以及

您所听到的关于

这些必须

截肢

的人的所有事情,这一切都是由大量炎症驱动的

,希望

像劳拉·莫玛布这样的药物

能够 对待它,但我们必须在

很长一段时间内潜在地对待它

,咆哮是告诉我们你

什么时候开始治疗的一个标志,因为

你什么时候做

ma 考虑从病毒性疾病到免疫性疾病的转变

以及您要治疗多长时间,但这

就是我们现在在医学上的能力

是提供药物并知道它在

做什么

我们不再将患者用作豚鼠

,让我们给这个 尝试

让我们尝试一下 我们知道何时

开始治疗 我们知道何时停止

治疗 最终不仅可以减轻

患者的

痛苦和痛苦,还可以节省医疗

保健费用

,我认为今天的其他一些谈话

将是 医疗保健

和covid的经济影响

,我们也必须考虑到,

因为我们正在

向前推进,呃,这些

方法中的一些,但我再次充满希望

,我希望我们有一种药物

一种能够消除死亡幽灵的疗法 消除

可怕疾病的幽灵

,使这只是另一种感染

,我们可以继续我们的工作

,恢复工作,恢复经济,

谢谢,我真的很感激 tedx

人邀请我在我的家乡

做这件事非常令人兴奋,

嗯,在

密歇根州北部的这个国家,嗯,

安全,我们正在努力,

非常感谢