Why bats dont get sick Arinjay Banerjee

If this bat were a human,
she’d be in deep trouble.

She’s infected with several
deadly viruses,

including ones that cause rabies,
SARS, and Ebola.

But while her diagnosis would be lethal
for other mammals,

this winged wonder is totally unfazed.

In fact, she may even spend
the next 30 years living

as if this were totally normal–
because for bats, it is.

So what’s protecting her
from these dangerous infections?

To answer this question,
we first need to understand

the relationship between
viruses and their hosts.

Every virus has evolved to infect specific
species within a class of creatures.

This is why humans are unlikely
to be infected by plant viruses,

and why bees don’t catch the flu.

However, viruses do sometimes jump
across closely related species

And because the new host
has no established immune defenses,

the unknown virus presents
a potentially lethal challenge.

This is actually bad news
for the virus as well.

Their ideal host provides a steady stream
of resources

and comes into contact with new parties
to infect—

two criteria that are best met
by living hosts.

All this to say that successful viruses

don’t typically evolve adaptations
that kill their hosts—

including the viruses that have infected
our flying friend.

The deadly effects of these viruses
aren’t caused by the pathogens directly,

but rather, by their host’s uncontrolled
immune response.

Infections like Ebola
or certain types of flu have evolved

to strain the immune system
of their mammalian host

by sending it into overdrive.

The body sends hordes
of white blood cells,

antibodies and inflammatory molecules
to kill the foreign invader.

But if the infection has progressed
to high enough levels,

an assault by the immune system
can lead to serious tissue damage.

In particularly virulent cases,
this damage can be lethal.

And even when it’s not,

the site is left vulnerable
to secondary infection.

But unlike other mammals,

bats have been in an evolutionary arms
race with these viruses for millennia,

and they’ve adapted to limit
this kind of self-damage.

Their immune system
has a very low inflammatory response;

an adaptation likely developed
alongside the other trait

that sets them apart from other mammals:
self-powered flight.

This energy-intensive process can raise
a bat’s body temperature to over 40ºC.

Such a high metabolic rate
comes at a cost;

flight produces waste molecules
called Reactive Oxygen Species

that damage and break off
fragments of DNA.

In other mammals, this loose DNA

would be attacked by the immune system
as a foreign invader.

But if bats produce these molecules
as often as researchers believe,

they may have evolved
a dampened immune response

to their own damaged DNA.

In fact, certain genes associated
with sensing broken DNA

and deploying inflammatory molecules
are absent from the bat genome.

The result is a controlled
low-level inflammatory response

that allows bats to coexist
with the viruses in their systems.

Even more impressive,

bats are able to host these viruses
for decades

without any negative health consequences.

According to a 2013 study, bats
have evolved efficient repair genes

to counteract the frequent
DNA damage they sustain.

These repair genes may also contribute
to their long lives.

Animal chromosomes end with a DNA sequence
called a telomere.

These sequences shorten over time
in a process

that many believe contributes
to cell aging.

But bat telomeres shorten much more slowly
than their mammalian cousins—

granting them lifespans
as long as 41 years.

Of course, bats aren’t totally
invincible to disease,

whether caused by bacteria,
unfamiliar viruses, or even fungi.

Bat populations have been ravaged
by a fungal infection

called white-nose syndrome,

which can fatally disrupt hibernation
and deteriorate wing tissue.

These conditions prevent bats
from performing critical roles

in their ecosystems, like helping
with pollination and seed dispersal,

and consuming pests and insects.

To protect these animals from harm,
and ourselves from infection,

humans need to stop encroaching
on bat habitats and ecosystems.

Hopefully, preserving these populations

will allow scientists to better understand
bats’ unique antiviral defense systems.

And maybe one day, this research will
help our own viral immunity take flight.

如果这只蝙蝠是人类,那
她就麻烦大了。

她感染了几种
致命病毒,

包括导致狂犬病、
非典和埃博拉病毒的病毒。

但是,虽然她的诊断
对其他哺乳动物来说是致命的,但

这个有翼的奇迹却完全不为所动。

事实上,她甚至可能
在接下来的 30 年里

过着完全正常的生活——
因为对于蝙蝠来说,就是这样。

那么是什么保护她
免受这些危险的感染呢?

要回答这个问题,
我们首先需要了解

病毒与宿主之间的关系。

每种病毒都已进化为感染
一类生物中的特定物种。

这就是为什么人类
不太可能被植物病毒感染,

以及蜜蜂不会感染流感的原因。

然而,病毒有时确实会
跨越密切相关的物种,

而且由于新宿主
没有建立免疫防御

,未知病毒提出
了潜在的致命挑战。

这实际上
对病毒来说也是个坏消息。

他们理想的宿主提供源源不断
的资源,

并与新的感染方接触——

这两个标准是
活着的宿主最能满足的。

所有这一切都表明,成功的病毒

通常不会进化
出杀死宿主的适应性——

包括感染
我们飞行朋友的病毒。

这些病毒的致命影响
不是由病原体直接引起的,

而是由宿主不受控制的
免疫反应引起的。

埃博拉病毒
或某些类型的流感等感染已经进化

到使
哺乳动物宿主

的免疫系统超负荷运转。

身体会发送成群
的白细胞、

抗体和炎症分子
来杀死外来入侵者。

但如果感染发展
到足够高的水平,

免疫系统的攻击
可能会导致严重的组织损伤。

在特别严重的情况下,
这种损害可能是致命的。

即使不是,

该网站也容易
受到二次感染。

但与其他哺乳动物不同,

蝙蝠
与这些病毒进行了数千年的进化军备竞赛

,它们已经适应了限制
这种自我伤害。

他们的免疫
系统的炎症反应非常低;

一种适应可能

使它们与其他哺乳动物区分开来的另一个特征一起发展:
自主飞行。

这种耗能的过程可以
将蝙蝠的体温提高到 40ºC 以上。

如此高的新陈代谢率
是有代价的。

飞行会产生一种
叫做活性氧的废物分子

,它们会破坏和破坏
DNA 片段。

在其他哺乳动物中,这种松散的 DNA

会被免疫系统
作为外来入侵者攻击。

但如果蝙蝠
像研究人员认为的那样频繁地产生这些分子,

它们可能已经进化

对自身受损 DNA 的免疫反应减弱。

事实上,蝙蝠基因组中不存在
与感知断裂 DNA

和部署炎症分子相关的某些
基因。

结果是一种受控的
低水平炎症反应

,使蝙蝠能够
与其系统中的病毒共存。

更令人印象深刻的是,

蝙蝠能够在
数十年内携带这些病毒,

而不会对健康造成任何负面影响。

根据 2013 年的一项研究,蝙蝠
已经进化出有效的修复基因

来抵消
它们经常遭受的 DNA 损伤。

这些修复基因也可能
有助于它们的长寿。

动物染色体以称为端粒的 DNA 序列结束

许多人认为会
导致细胞老化的过程中,这些序列会随着时间的推移而缩短。

但蝙蝠端粒的缩短速度
比它们的哺乳动物表亲要慢得多——

使它们的寿命
长达 41 年。

当然,

无论是由细菌、
不熟悉的病毒,甚至是真菌引起的,蝙蝠并非完全无敌。

蝙蝠种群
受到一种称为白鼻综合征的真菌感染的严重

破坏,这种疾病可以致命地破坏冬眠
并恶化翅膀组织。

这些条件阻止蝙蝠

在其生态系统中发挥关键作用,例如
帮助授粉和种子传播,

以及消耗害虫和昆虫。

为了保护这些动物免受伤害,保护
我们自己免受感染,

人类需要停止
侵犯蝙蝠栖息地和生态系统。

希望保存这些种群

将使科学家能够更好地了解
蝙蝠独特的抗病毒防御系统。

也许有一天,这项研究将
帮助我们自己的病毒免疫起飞。