the incurable bacterial infection that had ravaged Europe for centuries.

肆虐歐洲數百年的不治之症細菌感染。

Step 1: Infect patients suffering from the later stages of syphilis

第一步：感染梅毒晚期患者。

with the parasite that causes malaria,

與引起瘧疾的寄生蟲。

the deadly but curable mosquito-borne disease.

致命但可治癒的蚊子傳播疾病；

Step 2: Hope that malarial fevers clear the syphilis.

第二步：希望瘧疾發燒清除梅毒。

And step 3: Administer quinine to curb the malaria.

而第三步：注射奎寧，抑制瘧疾。

If all went according to plan,

如果一切按計劃進行。

their patient would be left alive and free of both diseases.

他們的病人會活著，沒有這兩種疾病。

This killed some 15% of patients, but for those who survived,

這使大約15%的病人死亡，但對於那些倖存下來的人來說。

it seemed to work.

似乎很有效。

It actually became the standard treatment for syphilis

它實際上成了梅毒的標準治療方法

until penicillin was widely used decades later.

直到幾十年後青黴素被廣泛使用。

And its driving force was fever.

而它的驅動力就是發燒。

There are many mysteries around fever,

圍繞著發燒，有很多奧祕。

but what we do know is that all mammals,

但我們知道的是，所有的哺乳動物，

some birds and even a few invertebrate and plant species feel fever's heat.

一些鳥類甚至一些無脊椎動物和植物物種都感受到了發燒的熱量。

It has persisted for over 600 million years of evolution.

在6億多年的進化過程中，它一直堅持著。

But it has a significant cost.

但它的成本很高。

For every 1 degree Celsius of temperature increase in the human body,

人體溫度每升高1攝氏度。

there's a 12.5 percent increase in energy required,

需要增加12.5%的能量。

the equivalent of about 20 minutes of jogging for some.

相當於一些人慢跑20分鐘左右。

So, why and how does your body produce a fever?

那麼，身體為什麼會產生髮燒，又是怎麼產生的呢？

Your core temperature is maintained via thermoregulation,

你的核心溫度是通過體溫調節來維持的。

a set of processes that usually keep you around 37 degrees Celsius.

一套流程，通常讓你保持在37攝氏度左右。

These mechanisms are controlled by the brain's hypothalamus,

這些機制由大腦的下丘腦控制。

which detects minute temperature shifts

檢測微小的溫度變化

and sends signals throughout the body accordingly.

並據此向全身發出信號。

If you're too hot, the hypothalamus produces signals

如果你太熱，下丘腦就會產生信號

that activate your sweat glands or make your blood vessels dilate,

激活你的汗腺或使你的血管擴張。

moving blood closer to the skin's surface—

使血液更接近皮膚表面------。

all of which releases heat and cools you off.

都會釋放熱量，給你降溫。

And if you're too cold,

而如果你太冷。

your blood vessels will constrict and you may start to shiver,

你的血管會收縮，你可能會開始發抖。

which generates heat.

產生熱量。

Your body will disrupt its usual temperature equilibrium to induce a fever,

你的身體會破壞平時的溫度平衡，誘發發燒。

which sets in above 38 degrees Celsius.

攝氏38度以上的集。

Meanwhile, it has mechanisms in place to prevent it

同時，它還建立了預防機制。

from exceeding 41 degrees Celsius, when organ damage could occur.

避免超過41攝氏度，否則會造成器官損傷。

Immune cells that are fighting an infection can induce a fever

正在與感染作鬥爭的免疫細胞會誘發發燒。

by triggering a biochemical cascade that ultimately instructs

通過觸發生化級聯，最終訓示了

your hypothalamus to increase your baseline temperature.

你的下丘腦增加你的基線溫度。

Your body then gets to work to meet its new “set point” using the mechanisms

然後，您的身體開始工作，以滿足其新的 "設定點"，使用機制。

it would to generate heat when cold.

它將產生熱時冷。

Until it reaches this new temperature, you'll feel comparatively cool,

在達到這個新的溫度之前，你會覺得比較涼爽。

which is why you might experience chills.

這就是為什麼你可能會經歷寒戰。

But why does your body do this?

但為什麼你的身體會這樣做呢？

While the jury's still out on how higher temperatures directly affect pathogens,

雖然陪審團仍在研究高溫如何直接影響病原體。

it seems that fever's main effect

看來，發燒的主要作用

is in rapidly inducing a whole-body immune response.

是在迅速誘發全身免疫反應。

Upon exposure to raised internal temperatures,

當接觸到內部溫度升高時。

some of your cells release heat shock proteins, or HSPs,

你的一些細胞會釋放熱休克蛋白，或HSPs。

a family of molecules produced in response to stressful conditions.

在應激條件下產生的一個分子家族。

These proteins aid lymphocytes, one of several kinds of white blood cells

這些蛋白質有助於淋巴細胞（白血球中的一種）的生長。

that fight pathogens, to travel more rapidly to infection sites.

抵抗病原體，更迅速地前往感染部位。

HSPs do this by enhancing the “stickiness” of lymphocytes,

HSPs通過增強淋巴細胞的 "粘性 "來實現。

enabling them to adhere to and squeeze through blood vessel walls

使它們能夠粘附並擠破血管壁

so they can reach the areas where infection is raging.

以便他們能夠到達感染肆虐的區域。

In the case of viral infections,

在病毒感染的情況下。

HSPs help tell nearby cells to dampen their protein production,

HSPs有助於告訴附近的細胞抑制其蛋白質的產生。

which limits their ability to replicate.

這限制了它們的複製能力。

This stunts the virus's spread because they depend on

這就阻礙了病毒的傳播，因為它們依賴於。

their host's replicative machinery to reproduce.

它們的宿主的複製機器進行繁殖。

It also protects surrounding cells from damage since some viruses spread

它還可以保護周圍的細胞不受損害，因為有些病毒會傳播。

by rupturing their host cells, which can lead to large-scale destruction,

通過破壞其宿主細胞，從而導致大規模的破壞。

the build-up of detritus, and potentially even organ damage.

雜物的堆積，甚至有可能造成器官損傷。

The ability of HSPs to protect host cells and enhance immune activity

HSPs保護宿主細胞和增強免疫活動的能力。

can limit the pathogen's path of destruction inside of the body.

可以限制病原體在體內的破壞路徑。

But for all we know about fever's role in immune activation,

但對於我們所知道的發熱在免疫激活中的作用。

some clinical trials have shown that fever suppressor drugs

一些臨床試驗表明，退燒藥

don't worsen symptoms or recovery rates.

不要使症狀或恢復率惡化。

This is why there's no definitive rule on whether to suppress a fever

這也是為什麼發燒要不要退燒沒有定論的原因。

or let it ride.

或讓它騎。

Doctors decide on a case-by-case basis.

醫生根據具體情況決定。

The fever's duration and intensity, as well as their patient's immune status,

發熱的持續時間和強度，以及他們患者的免疫狀態。

comfort level, and age will all play a role in their choice of treatments.

舒適度和年齡都會對他們選擇治療方法產生影響。

And if they do let a fever ride,

如果他們真的讓發燒了。

they'll likely prescribe rest and plenty of fluids to prevent dehydration

他們可能會開出休息和大量的液體，以防止脫水。

while the body wages its heated battle.

而身體卻在進行著激烈的戰鬥。