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拿感冒沒辦法?科學家另闢蹊徑對抗感冒病毒

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Scientists think they have found a way to stop the common cold and closely related viruses which can cause paralysis.

科學家們認爲他們已經找到了一種方法來治療普通感冒以及與其密切相關的病毒,這些病毒可能導致癱瘓。

Instead of trying to attack them directly, the researchers targeted an essential protein inside our cells which the viruses need to replicate.

研究人員沒有試圖直接攻擊感冒病毒,而是將研究目標對準了病毒複製所需的細胞內的一種基本蛋白質。

The approach gave "complete protection" in experiments on mice and human lung cells.

該方法在針對小鼠和人類肺細胞的實驗中提供了“完全的保護”。

However, the US-based researchers are not ready for trials in people.

不過,美國的研究人員還沒有準備好進行人體試驗。

Tackling the common cold has been a massive problem in medicine.

治療普通感冒一直是醫學界的一大難題。

Most colds are caused by rhinoviruses, but there are around 160 different types and they mutate so easily they rapidly become resistant to drugs, or learn to hide from the immune system.

大多數感冒由鼻病毒引起,但是大約有160種不同的病毒,它們很容易變異,並且會迅速產生抗藥性,或者學會躲避免疫系統。

This has led to the idea of "host-directed therapy" - essentially making our bodies inhospitable for the cold viruses.

這引發了“宿主導向療法”的想法,也就是從本質上使人的身體不適合感冒病毒存活。

An individual virus does not have everything it needs to replicate. Instead, it is dependent on infecting another cell and stealing some of the parts inside.

單個病毒並不具備複製所需的一切。相反,它依賴於感染另一個細胞並從中獲取部分物質。

It is why scientists still argue whether viruses are truly alive.

因此,科學家們仍然在爭論病毒是否真的是活的。

A team at Stanford University and the University of California, San Francisco, found one of the components which the viruses were dependent upon.

斯坦福大學和加州大學舊金山分校的一個研究小組發現了病毒所依賴的一種成分。

Scientists started with human cells and then used gene-editing to turn off instructions inside our DNA one-by-one.

科學家從人類細胞開始,之後用基因編輯一個接一個地關閉人類DNA中的指令。

These modified cells were then exposed to a range of enteroviruses - this includes the rhinoviruses which cause the common cold, and more dangerous viruses that are closely related to polio and can cause paralysis.

這些經過編輯的細胞隨後暴露在多種腸道病毒中——包括導致普通感冒的鼻病毒,以及與脊髓灰質炎密切相關、可能導致癱瘓的更危險的病毒。

All the viruses were unable to replicate inside cells which had the instructions for a protein (called methyltransferase SETD3) switched off.

所有的病毒都無法在細胞內複製,因爲這些細胞內的一種蛋白質(甲基轉移酶SETD3)的指令已經關閉。

The scientists then created genetically modified mice which were completely unable to produce that protein.

然後,科學家們創造了完全不能產生這種蛋白質的轉基因老鼠。

"Lacking that gene protected the mice completely from viral infection," associate professor Jan Carette, from Stanford, told the BBC.

斯坦福大學的副教授簡·凱瑞特告訴英國廣播公司說:“缺乏這種基因使老鼠完全免受病毒感染。”

"These mice would always die [without the mutation], but they survived and we saw a very strong reduction in viral replication and very strong protection."

“如果沒有突變,這些小鼠總是會死亡,但它們存活了下來。我們看到病毒複製大幅減少,保護作用非常強。”

拿感冒沒辦法?科學家另闢蹊徑對抗感冒病毒

The protein these viruses were dependent upon normally has a role in the intricate "scaffolding" which organises the inside of the body's cells, called the cytoskeleton.

這些病毒所依賴的蛋白質通常在複雜的“支架”中發揮作用,“支架”負責組織體內的細胞,被稱爲細胞骨架。

The findings, published in the journal Nature Microbiology, showed the genetically modified mice were healthy, despite lacking the protein for their whole lives.

這項研究結果發表在《自然微生物學》期刊上。結果顯示,儘管轉基因小鼠終生缺乏這種蛋白質,但它們是健康的。

The plan is not to produce genetically modified humans, but to find a drug which can temporarily suppress the protein, and provide protection.

科學家的目的並不是打造轉基因人類,而是尋找一種能暫時抑制這種蛋白質並提供保護的藥物。

"We have identified a fantastic target that all enteroviruses and rhinoviruses require and depend on. Take that away and the virus really has no chance," said Prof Carette.

“我們已經確定了所有腸病毒和鼻病毒都需要和依賴的一個極好的靶點。如果把它清除掉,病毒就沒有機會興風作浪了,”凱瑞特教授說。

He added: "This is a really good first step - the second step is to have a chemical that mimics this genetic deletion.

他補充說:“這是非常好的第一步,第二步是找到可以模仿這種基因缺失的化學物質。”

"I think development can go relatively quickly."

“我認爲進展相對會比較快。”

Exactly what role the protein plays in the viral replication is still uncertain, and will require further research.

這種蛋白質在病毒複製中究竟起什麼作用尚不清楚,還需進一步研究。

For most people the common cold is more of an inconvenience than a threat to their health, but in asthmatics it can make their symptoms much worse and some of the enteroviruses can causes paralysis if they spread to the brain.

對大多數人來說,普通感冒對健康與其說是一種威脅,不如說是一種不便,但對哮喘患者來說,感冒會加劇症狀,而一些腸道病毒如果傳播到大腦,可能會導致癱瘓。

Prof Jonathan Ball, a virologist at the University of Nottingham, who was not involved in the work, said the study was "neat" but scientists would need to be certain the approach was safe.

諾丁漢大學病毒學家喬納森·鮑爾教授沒有參與這項研究,他表示,這項研究“很簡潔”,但科學家需要確定這種方法是安全的。

"There is increasing interest in developing treatments that target these host proteins, because it can potentially overcome virus mutation - one of the major barriers to developing effective broadly active antivirals.

“人們對研發針對這些宿主蛋白質的治療方法越來越感興趣,因爲它可能克服病毒突變——這是研發有效的廣譜抗病毒藥物的主要障礙之一。

"But of course, viruses are very adaptable and it is conceivable that even a host-targeting treatment might not keep them at bay for long."

“當然,病毒適應性很強,可以想象,即使是針對宿主的治療也可能無法長期控制它們。”