How do viruses jump from animals to humans Ben Longdon

At a Maryland country fair in 2017,

the prize pigs were not
looking their best.

Farmers reported feverish hogs with
inflamed eyes and running snouts.

But while fair officials worried
about the pigs,

the Maryland department of health was
concerned about a group of sick fairgoers.

Some had pet the pigs, while others had
merely been near their barns;

but soon, 40 of these attendees would
be diagnosed with swine flu.

More often than not, sick animals
don’t infect humans.

But when they do, these
cross-species infections,

or viral host jumps,

have the potential to produce
deadly epidemics.

So how can pathogens from one species
infect another,

and what makes host jumps so dangerous?

Viruses are a type of organic parasite
infecting nearly all forms of life.

To survive and reproduce, they must move
through three stages:

contact with a susceptible host,
infection and replication,

and transmission to other individuals.

As an example, let’s look
at human influenza.

First, the flu virus encounters
a new host

and makes its way into
their respiratory tract.

This isn’t so difficult, but to survive
in this new body,

the virus must mount a successful
infection

before it’s caught and broken down
by an immune response.

To accomplish this task,

viruses have evolved specific interactions
with their host species.

Human flu viruses are covered in proteins

adapted to bind with matching receptors
on human respiratory cells.

Once inside a cell, the virus employs
additional adaptations

to hijack the host cell’s reproductive
machinery

and replicate its own genetic material.

Now the virus only needs to suppress
or evade the host’s immune system

long enough to replicate to sufficient
levels and infect more cells.

At this point, the flu can be passed on to
its next victim

via any transmission
of infected bodily fluid.

However, this simple sneeze also brings
the virus in contact with pets,

plants, or even your lunch.

Viruses are constantly encountering
new species and attempting to infect them.

More often than not, this ends in failure.

In most cases, the genetic dissimilarity
between the two hosts is too great.

For a virus adapted to infect humans,

a lettuce cell would be a foreign and
inhospitable landscape.

But there are a staggering number
of viruses circulating in the environment,

all with the potential to
encounter new hosts.

And because viruses rapidly reproduce
by the millions,

they can quickly develop random mutations.

Most mutations will have no effect,
or even prove detrimental;

but a small proportion may enable the
pathogen to better infect a new species.

The odds of winning this destructive
genetic lottery increase over time,

or if the new species is closely related
to the virus’ usual host.

For a virus adapted to another mammal,

infecting a human might just take
a few lucky mutations.

And a virus adapted to chimpanzees,

one of our closest genetic relatives,
might barely require any changes at all.

It takes more than time and genetic
similarity

for a host jump to be successful.

Some viruses come equipped to easily
infect a new host’s cells,

but are then unable to evade
an immune response.

Others might have a difficult time
transmitting to new hosts.

For example, they might make the host’s
blood contagious,

but not their saliva.

However, once a host jump reaches
the transmission stage,

the virus becomes much more dangerous.

Now gestating within two hosts,

the pathogen has twice the odds of
mutating into a more successful virus.

And each new host increases
the potential for a full-blown epidemic.

Virologists are constantly looking for
mutations

that might make viruses such as influenza
more likely to jump.

However, predicting the next potential
epidemic is a major challenge.

There’s a huge diversity of viruses
that we’re only just beginning to uncover.

Researchers are tirelessly studying the
biology of these pathogens.

And by monitoring populations to quickly
identify new outbreaks,

they can develop vaccines and containment
protocols to stop these deadly diseases.

在 2017 年马里兰州的一个乡村集市上

,获奖猪
看起来并不是最好的。

农民报告说,猪发烧,
眼睛发炎,流鼻涕。

但是,尽管展会官员
担心这些猪,

但马里兰州卫生部却
担心一群生病的展会观众。

有些人抚摸过猪,有些人
只是在他们的谷仓附近;

但很快,这些与会者中有 40 人将
被诊断出患有猪流感。

通常情况下,生病的动物
不会感染人类。

但是当他们这样做时,这些
跨物种感染

或病毒宿主跳跃,

有可能产生
致命的流行病。

那么,一个物种的病原体如何感染另一个物种

又是什么让宿主跳跃如此危险?

病毒是一种有机寄生虫,
几乎可以感染所有形式的生命。

为了生存和繁殖,它们必须
经历三个阶段:

与易感宿主接触、
感染和复制

以及传播给其他个体。

例如,让我们
看看人类流感。

首先,流感病毒
遇到新宿主

并进入
其呼吸道。

这并不难,但要
在这个新身体中生存

,病毒必须

在被免疫反应捕获和分解之前成功感染

为了完成这项任务,

病毒已经进化出
与其宿主物种的特定相互作用。

人类流感病毒被蛋白质覆盖,这些蛋白质

适合与
人类呼吸细胞上的匹配受体结合。

一旦进入细胞,病毒就会利用
额外的适应性

来劫持宿主细胞的生殖
机制

并复制其自身的遗传物质。

现在病毒只需要抑制
或逃避宿主的免疫系统

足够长的时间就可以复制到足够的
水平并感染更多的细胞。

此时,流感可以

通过任何
受感染的体液传播传染给下一个受害者。

然而,这种简单的喷嚏也
会使病毒与宠物、

植物甚至您的午餐接触。

病毒不断遇到
新物种并试图感染它们。

这往往以失败告终。

在大多数情况下,
两个宿主之间的遗传差异太大。

对于适应感染人类的病毒来说

,生菜细胞将是一个陌生而
荒凉的环境。

但是
在环境中传播的病毒数量惊人,

所有这些病毒都有可能
遇到新的宿主。

而且由于病毒
以数百万的速度快速繁殖,

它们可以迅速产生随机突变。

大多数突变不会产生影响,
甚至被证明是有害的;

但一小部分可能会使
病原体更好地感染新物种。

赢得这种破坏性
基因彩票的几率会随着时间的推移而增加,

或者如果新物种
与病毒的通常宿主密切相关。

对于适应另一种哺乳动物的病毒,

感染人类可能只
需要一些幸运的突变。

而一种适应黑猩猩的病毒

,我们最亲近的遗传亲属之一,
可能几乎不需要任何改变。

宿主跳跃成功需要的不仅仅是时间和遗传
相似

性。

一些病毒具备轻松
感染新宿主细胞的能力,

但无法逃避
免疫反应。

其他人可能难以
传输到新主机。

例如,它们可能会使宿主的
血液具有传染性,

但不会使它们的唾液具有传染性。

然而,一旦宿主跳跃
达到传播阶段

,病毒就会变得更加危险。

现在在两个宿主体内孕育

,病原体
变异成更成功病毒的几率是原来的两倍。

每个新宿主都增加
了全面流行病的可能性。

病毒学家一直在寻找

可能使流感等病毒
更容易跳跃的突变。

然而,预测下一次潜在的
流行病是一项重大挑战。

我们才刚刚开始发现各种各样的病毒。

研究人员正在不知疲倦地研究
这些病原体的生物学。

通过监测人群以快速
识别新的爆发,

他们可以开发疫苗和遏制
协议来阻止这些致命的疾病。