一種準備跨越物種傳播給人類的病毒

資料來源：F. Perry Wilson，醫學博士，臨床流病理學碩士 / 2022 年 10 月 4 日 / Medscape / 財團法人台灣紅絲帶基金會編譯

 

歡迎來到影響因子，這是您對一項新醫學研究的每週評論。我是耶魯大學醫學院的 F. Perry Wilson 博士。

今天，我在這片幽暗的森林裡——或者我能在康乃狄克州郊區找到那片幽暗的森林——談論病毒以及它們如何從動物身上跳到人類身上。病毒的人畜共通疾病傳播是造成許多流行病和大流行病的原因，當然包括最近的 SARS-CoV-2 大流行。但它以前發生過，而且還會再次發生。

我喜歡我今天想和你談談的這篇論文的原因是，作者強調了在動物宿主中存在的病毒要跳入人類需要做的四件事。因為一旦我們知道這四件事是什麼，我們就可以識別出接近滿足這些標準的病毒並密切關注它們。

研究人員用來教我們有關於人畜共通疾病傳播的實物課是動脈炎病毒。

 

圖 1：細胞期刊

 

這是一個 RNA 病毒家族，與我們所知道和喜愛的冠狀病毒並沒有太遠的關係。具體來說，他們專注於一種叫做猿猴出血熱病毒（SHFV）的東西。例如，這是一種像伊波拉病毒一樣的出血熱病毒，伊波拉當然已經從動物宿主轉變為人類宿主。但 SHFV 尚未離開它的主要物種，即舊大陸的猴子，而跳躍到人類。

 

圖 2：維基百科

 

那麼，生活在其他動物體內的病毒需要做什麼才能進入人類？像猿猴出血熱病毒（SHFV）的距離有多近，以及若擴及許多動脈炎病毒呢？

為了能夠感染細胞，病毒必須進入。正如作者透過一些很好的實驗所顯示的那樣，SHFV 使用一種稱為 CD163 的細胞受體，它是一種重要的細胞受體。我們需要它，當紅血球分解時，它有助於清除血紅素。例如，它在巨噬細胞和單核細胞上。該病毒附著在猴子宿主上的一個非常相似的受體上，研究人員顯示，它基本上沒有任何問題附著在人類 CD163 上，從而感染細胞。那裡並沒有障礙。

 

圖 3：細胞期刊

 

真正有趣的是，他們觀察了各種舊大陸猴子，實際上它們中的許多已經進化出它們的 CD163 受體，使其不易受到感染。

 

圖 4：細胞期刊

 

但是人類，因為我們沒有感受到這種病毒的選擇性壓力，所以我們的 CD163 真的沒有進化去防禦。它完全有能力綁定這種病毒，這令人擔憂。

第二，一旦病毒進入細胞，這還不夠。它必須使用細胞機器來複製更多的病毒。

 

圖 5：細胞期刊

 

動脈炎病毒可以使用人類細胞生產方法來複製更多的病毒嗎？研究人員對此進行了調查。正如你在這裡看到的，這並沒有任何問題。

這些病毒可以在人體細胞內很好地複制。

第三是先天免疫。

 

圖 6：細胞期刊

 

就病毒而言，這基本上是干擾素。這些是我們為抵禦多種病毒而生產的物質。它們是我們與生俱來的。我們以前不必見過這種病毒。不幸的是，干擾素似乎並不是 SHFV 複製的特殊障礙。

最後，第四個是適應性免疫。

 

圖 7：細胞期刊

 

我們以前見過這種病毒嗎？因此，如果我們再次被感染，我們是否有一些記憶 T 和 B 細胞準備好開始行動？並沒有人類獲得適應性免疫的真正證據，因為這種病毒根本沒有被證明已經進入人類。這裡顯然與 SARS-CoV-2 有相似之處，因為當 SARS-CoV-2 出現時，基本上沒有人具有任何適應性免疫，因為它是新穎的。

這裡的底線是，不——我們不會太擔心 SHFV。但是，生活在所有舊大陸猴子身上的這些類型的動脈炎病毒非常接近能夠從猴子躍遷到人類身上。隨著人類更深入地侵入他們的環境，他們將越來越多地與這些特定病毒的動物宿主接觸。

 

圖 8：Pexels

 

我們知道我們需要注意哪些方面，對於可能能夠實現跳躍的病毒。作者認為，我們應該進行人口上的監視，開發血清學測試，看看是否發生了這種跳躍，這樣我們就可以足夠快地採取行動，並在下一次大流行開始之前阻止它。

 

F. Perry Wilson，醫學博士，臨床流病理學碩士(MSCE)，是醫學副教授，耶魯大學臨床和轉化研究加速器主任。他的科學傳播工作可以在赫芬頓郵報、美國國家公共電台(NPR) 和 Medscape 上找到。

© 2022 WebMD, LLC

引用：F. Perry Wilson。一種準備跨越物種傳播給人類的病毒 – Medscape – 2022 年 10 月 4 日。

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

A Virus Poised to Jump Species to Humans

F. Perry Wilson, MD, MSCE / October 04, 2022 / Medscape

 

Welcome to Impact Factor, your weekly dose of commentary on a new medical study. I’m Dr F. Perry Wilson of the Yale School of Medicine.

Today I’m here in the deep, dark forest — or as close as I can find the deep, dark forest in suburban Connecticut — to talk about viruses and how they can jump from animals into humans. The zoonotic transmission of viruses is responsible for a host of epidemics and pandemics, including, of course, the most recent SARS-CoV-2 pandemic. But it’s happened before, and it will happen again.

What I love about the paper I want to talk to you about today is that the authors highlight four things that a virus that exists in an animal reservoir needs to be able to do to jump into humans. Because once we know what these four things are, we can identify viruses that are close to meeting these criteria and keep an eye out for them.

The object lesson that the researchers are using to teach us about zoonotic transmission is arteriviruses.

 

Image 1: Cell

 

This is a family of RNA viruses, which is not too distantly related to the coronaviruses that we know and love. Specifically, they’re focusing on something called simian hemorrhagic fever virus (SHFV). This is a hemorrhagic fever virus like Ebola, for example, which, of course, has made the transition from animals into human hosts. But SHFV has not left its primary species, which is an Old World monkey, to jump into humans yet.

 

Image 2: Wikipedia

 

So, what does a virus that lives in some other animal need to be able to do to get into humans? And how close is SHFV, and by extension, many of the arteriviruses?

To be able to infect a cell, a virus has to get in. The SHFV, as the authors show through some nice experiments, uses a cellular receptor called CD163, which is an important cellular receptor. We need it. It helps scavenge heme groups as red blood cells break down. It’s on macrophages and monocytes, for example. The virus attaches to a very similar receptor on the monkey host, and the researchers show that it has basically no problem whatsoever attaching to human CD163 and thereby infecting cells. No barrier there.

 

Image 3: Cell

 

What’s really interesting about this is that they looked at a variety of Old World monkeys, and actually many of them have evolved their CD163 receptors to be less susceptible to infection.

 

Image 4: Cell

 

But humans, because we haven’t been under selective pressure from this virus, have really no evolutionary defense built into our CD163. It’s fully capable of binding this virus, which is concerning.

Number two, once a virus gets into a cell, that’s not enough. It must use the cellular machinery to make more copies of itself.

 

Image 5: Cell

 

Can arteriviruses use human cellular production methods to make more copies of themselves? The researchers investigated this. And as you can see here, it’s no problem whatsoever.

These viruses can do just fine replicating inside human cells.

Number three is innate immunity.

 

Image 6: Cell

 

This is basically, in the case of viruses, interferon. These are substances that we produce to defend against a broad variety of viruses. They’re innate to us. We don’t have to have seen the virus before. And unfortunately, interferon does not seem to be a particular barrier to replication of SHFV.

And finally, number four is adaptive immunity.

 

Image 7: Cell

 

Have we seen this virus before, and thus, do we have some memory T and B cells there that are ready to leap into action should we become infected again? There’s no real evidence of adaptive immunity in humans because this virus has never been shown to have entered humans at all. There’s clearly a parallel here with SARS-CoV-2 in that basically no one had any adaptive immunity when SARS-CoV-2 emerged because it was novel.

The bottom line here is, no — we’re not going to worry too much about SHFV. But these classes of arteriviruses, which live in all Old World monkeys, are very close to being able to leap from monkey to human. As humans encroach deeper into their environment, they’re going to come into contact more and more with these animal reservoirs of certain viruses.

 

Image 8: Pexels

 

We know what aspects we need to be on the lookout for, for viruses that may be able to make the jump. And the authors argue that we should be surveilling the human population, developing serology tests to see if that jump has been made, so we can act quickly enough and stop the next pandemic before it starts.

For Medscape, I’m Perry Wilson.

 

F. Perry Wilson, MD, MSCE, is an associate professor of medicine and director of Yale’s Clinical and Translational Research Accelerator. His science communication work can be found in the Huffington Post, on NPR, and here on Medscape. 

Medscape © 2022 WebMD, LLC

Cite this: F. Perry Wilson. A Virus Poised to Jump Species to Humans – Medscape – Oct 04, 2022.