What is a coronavirus Elizabeth Cox

For almost a decade, scientists chased
the source of a deadly new virus

through China’s tallest mountains
and most isolated caverns.

They finally found it here:
in the bats of Shitou Cave.

The virus in question was a coronavirus

that caused an epidemic
of severe acute respiratory syndrome,

or SARS, in 2003.

Coronaviruses are a group of viruses

covered in little protein spikes
that look like a crown—

or “corona” in Latin.

There are hundreds
of known coronaviruses.

Seven of them infect humans,
and can cause disease.

The coronavirus SARS-CoV causes SARS,
MERS-CoV causes MERS,

and SARS-CoV-2 causes
the disease COVID-19.

Of the seven human coronaviruses,
four cause colds,

mild, highly contagious infections
of the nose and throat.

Two infect the lungs,
and cause much more severe illnesses.

The seventh, which causes COVID-19,
has features of each:

it spreads easily,
but can severely impact the lungs.

When an infected person coughs,
droplets containing the virus spray out.

The virus can infect a new person when
the droplets enter their nose or mouth.

Coronaviruses transmit best
in enclosed spaces,

where people are close together.

Cold weather keeps their delicate casing
from drying out,

enabling the virus to survive
for longer between hosts,

while UV exposure from sunlight
may damage it.

These seasonal variations matter more
for established viruses.

But because no one is yet immune
to a new virus,

it has so many potential hosts that it
doesn’t need ideal conditions to spread.

In the body, the protein spikes embed
in the host’s cells and fuse with them—

enabling the virus to hijack
the host cell’s machinery

to replicate its own genes.

Coronaviruses store their genes on RNA.

All viruses are either RNA viruses
or DNA viruses.

RNA viruses tend to be smaller,
with fewer genes,

meaning they infect many hosts
and replicate quickly in those hosts.

In general, RNA viruses don’t have
a proofreading mechanism,

whereas DNA viruses do.

So when an RNA virus replicates,

it’s much more likely to have
mistakes called mutations.

Many of these mutations are useless
or even harmful.

But some make the virus better suited
for certain environments—

like a new host species.

Epidemics often occur when a virus
jumps from animals to humans.

This is true of the RNA viruses
that caused

the Ebola, Zika, and SARS epidemics,
and the COVID-19 pandemic.

Once in humans, the virus still mutates—

usually not enough to create a new virus,

but enough to create variations,
or strains, of the original one.

Coronaviruses have a few key differences
from most RNA viruses.

They’re some of the largest,
meaning they have the most genes.

That creates more opportunity
for harmful mutations.

To counteract this risk,
coronaviruses have a unique feature:

an enzyme that checks for replication
errors and corrects mistakes.

This makes coronaviruses
much more stable,

with a slower mutation rate,
than other RNA viruses.

While this may sound formidable,

the slow mutation rate
is actually a promising sign

when it comes to disarming them.

After an infection, our immune systems
can recognize germs

and destroy them more quickly
if they infect us again

so they don’t make us sick.

But mutations can make a virus
less recognizable to our immune systems—

and therefore more difficult to fight off.

They can also make antiviral drugs
and vaccines less effective,

because they’re tailored
very specifically to a virus.

That’s why we need a new flu vaccine
every year—

the influenza virus mutates so quickly
that new strains pop up constantly.

The slower mutation rate
of coronaviruses means

our immune systems, drugs,
and vaccines

might be able to recognize them
for longer after infection,

and therefore protect us better.

Still, we don’t know how long our bodies
remain immune to different coronaviruses.

There’s never been an approved treatment
or vaccine for a coronavirus.

We haven’t focused on treating
the ones that cause colds,

and though scientists began developing
treatments for SARS and MERS,

the epidemics ended before those
treatments completed clinical trials.

As we continue to encroach
on other animals’ habitats,

some scientists say a new coronavirus
jumping to humans is inevitable—

but if we investigate these unknowns,
it doesn’t have to be devastating.

近十年来,科学家们

中国最高的山脉
和最孤立的洞穴中寻找一种致命的新病毒的来源。

他们终于在这里找到了:
石头洞的蝙蝠。

有问题的病毒是一种冠状

病毒,它在 2003 年引起了
严重急性呼吸系统综合症

或 SARS 的流行。

冠状病毒是一组

覆盖着小蛋白质尖峰的病毒
,看起来像一个皇冠——

或拉丁语中的“冠状病毒”。

已知的冠状病毒有数百种。

其中七种会感染人类,
并可能导致疾病。

冠状病毒 SARS-CoV 导致 SARS,
MERS-CoV 导致 MERS

,SARS-CoV-2
导致疾病 COVID-19。

在七种人类冠状病毒中,有
四种会引起感冒、

轻微、高度传染性
的鼻子和喉咙感染。

两个感染肺部,
并导致更严重的疾病。

第七种导致 COVID-19 的病毒
具有每种

病毒的特征:它很容易传播,
但会严重影响肺部。

当感染者咳嗽时,会
喷出含有病毒的飞沫。

当飞沫进入新人的鼻子或嘴巴时,病毒会感染新人。

冠状病毒

在人们靠近的封闭空间传播得最好。

寒冷的天气可以防止它们脆弱的外壳
变干,

从而使病毒
在宿主之间存活更长时间,

而阳光下的紫外线照射
可能会损坏它。

这些季节性变化
对已建立的病毒更为重要。

但由于目前还没有人
对一种新病毒免疫,

它有很多潜在的宿主,
不需要理想的传播条件。

在体内,蛋白质尖峰
嵌入宿主细胞并与它们融合——

使病毒能够
劫持宿主细胞的机制

来复制自己的基因。

冠状病毒将它们的基因存储在 RNA 上。

所有病毒要么是 RNA 病毒,
要么是 DNA 病毒。

RNA病毒往往更小
,基因更少,

这意味着它们会感染许多宿主
并在这些宿主中快速复制。

一般来说,RNA病毒
没有校对机制,

而DNA病毒有。

因此,当 RNA 病毒复制时,

它更有可能
出现称为突变的错误。

许多这些突变是无用的
,甚至是有害的。

但有些使病毒更
适合某些环境——

比如新的宿主物种。

当病毒从动物传播到人类时,通常会发生流行病

导致埃博拉病毒、寨卡病毒和 SARS 流行病
以及 COVID-19 流行病的 RNA 病毒也是如此。

一旦进入人体,病毒仍然会发生变异——

通常不足以产生新病毒,

但足以产生
原始病毒的变异或毒株。

冠状病毒
与大多数 RNA 病毒有一些关键区别。

它们是最大的,
这意味着它们拥有最多的基因。

这为有害突变创造了更多机会

为了抵消这种风险,
冠状病毒具有一个独特的功能:

一种检查复制
错误并纠正错误的酶。

这使得冠状病毒
比其他 RNA 病毒更稳定

,突变率更慢

虽然这听起来很可怕,但在解除它们的武装时,

缓慢的突变
率实际上是一个有希望的迹象

感染后,我们的免疫系统
可以识别细菌


在它们再次感染我们时更快地消灭它们,

这样它们就不会让我们生病。

但是突变会使
我们的免疫系统无法识别病毒

,因此更难以抵抗。

它们还可以降低抗病毒药物
和疫苗的效果,

因为它们是专门针对病毒量身定制
的。

这就是为什么我们每年都需要一种新的流感疫苗——

流感病毒变异得如此之快
,以至于新毒株不断出现。

冠状病毒较慢的突变
率意味着

我们的免疫系统、药物
和疫苗在感染后

可能能够识别它们
的时间更长

,从而更好地保护我们。

不过,我们不知道我们的身体
对不同的冠状病毒免疫多久。

从未有过
批准的冠状病毒治疗方法或疫苗。

我们并没有专注于
治疗引起感冒的疾病

,尽管科学家们开始开发
治疗 SARS 和 MERS 的方法,

但在这些治疗方法完成临床试验之前,流行病就结束了

随着我们继续
侵占其他动物的栖息地,

一些科学家说,一种新的冠状病毒会
传染给人类是不可避免的——

但如果我们调查这些未知数,
它不一定是毁灭性的。