Though not technically alive, viruses mutate and evolve similar to living cells, producing new variants all the time.Without genetic mutations, there would be no humans. There wouldn’t be any living beings at all—no mammals, insects, or plants, not even bacteria.
雖然原則上並不活躍。不過，病毒變異及演化類似活細胞，一直在產生新變異體。沒有基因突變，就不會有人類。根本不會有任何生物——沒有哺乳動物、昆蟲或植物，甚至沒有細菌。
These tiny errors, which can happen at random each time a cell or virus copies itself, provide the raw materials for evolution to take place. Mutations create variation in a population, which allows natural selection to amplify the traits that help creatures thrive—stretching a giraffe’s long neck to reach high leaves, or camouflaging caterpillars like poop to evade birds’notice.
每次細胞或病毒自行複製時，隨機發生的上述微小差錯，為發生演化提供了原材料。突變會在種群中產生，使自然淘汰(物競天擇)得以增強，有助於生物茁壯成長之特徵的變異——伸展長脖子，來及於高處葉子的長頸鹿，或偽裝如糞便，以逃避鳥類注意的毛毛蟲。
Amid a pandemic, however, the word “mutation” strikes a more ominous note. Viruses, though not technically alive, also mutate and evolve as they infect a hosts’ cells and replicate. The resulting tweaks to the virus’s genetic code could help it more readily hop between humans or evade the defenses of the immune system. Three such mutants of the virus SARS-CoV-2 have prompted experts to advocate for redoubled efforts to curb the coronavirus’s spread.
不過，在大流行病中，“突變”該詞觸發一種，較為不祥的意味。雖然原則上並不活躍，不過感染宿主細胞及複製時，病毒也發生變異及演化。從而對病毒遺傳密碼產生的諸多調整，可能協助其在人類之間更迅速跳躍，或避開免疫系統的防禦。第二型嚴重急性呼吸系統徵候群-冠狀病毒(SARS-CoV-2：Severe Acute Respiratory Syndrome Coronavirus-2)的三個此類突變體，促使了專家們鼓吹加倍努力，來遏制冠狀病毒的傳播。
But these three versions of the virus are just a few among thousands of SARS-CoV-2 variants that have sprung up since the pandemic began. “We are creating variants like gangbusters right now because we have so many humans infected with SARS CoV-2,”says Siobain Duffy, a vial evolutionary biologist at Rutgers School of Environmental and Biological Sciences.
不過，該種病毒的上述三個版本，只是打從此大流行病開始以來，已經湧現之數千種SARS-CoV-2變異體中的少數。美國羅格斯大學環境暨生物科學學院，病毒演化生物學家，Siobain Duffy宣稱:「目前，人類正在引起諸多，類似黑幫剋星(gangbuster)的變異體。因為，有太多人類感染上SARS CoV-2。」
Many of these variants have since vanished. So why do some versions disappear, and why does the virus change in the first place? What mechanisms play puppet master for evolving viruses?
諸多這些變異體已經消失。那麼，究竟為何有些版本消失，及為何此病毒發生改變？什麼機制扮演了，演化中之病毒的傀儡大師？
“The virus will change because that’s the underlying biology,”says Simon Anthony, a virologist working in infectious diseases at the University of California, Davis.“The question then becomes, are those changes significant to us?”
美國加州大學戴維斯分校，從事傳染病研究的病毒學家，Simon Anthony宣稱:「該種病毒會發生改變，因為那是基本的生命現象。那麼，問題成為，那些改變對人類意義重大嗎？」
A successful virus is one that makes more of itself. But these tiny entities can’t do much on their own. Viruses are essentially coils of genetic material stuffed into a protein shell that’s sometimes blanketed in an outer envelope. In order to replicate, they must find a host. The virus binds to its target’s cells, injecting genetic material that hijacks the host’s cellular machinery to make a new generation of viral progeny.
興旺的病毒是種，能產生更多自身的病毒。不過，此些微小實體靠自己，無法產生很多。本質上，病毒是被填塞進入，有時被覆蓋於一層外包膜之蛋白質外殼中的數圈遺傳物質。為了複製，它們必須找到宿主。病毒與其標的細胞結合，並注入劫持宿主的細胞機制，來產生新一代之病毒後代的遺傳物質。
But each time a new copy is made, there’s a chance that an error, or mutation, will occur. Mutations are like typos in the string of “letters” that make up a strand of DNA or RNA code.
不過，每次產生新複製物時，皆有會發生差錯或突變的可能性。突變類似，組成一串DNA或RNA密碼之“鹼基”(由C、G、A、T，及U五個字母代表)串中的排列錯誤。
The majority of mutations are harmful to a virus or cell, limiting the spread of an error through a population. For example, mutations can tweak the building blocks of proteins encoded in the DNA or RNA, which alters a protein’s final shape and prevents it from doing its intended job, Duffy explains.
Duffy解釋，大多數突變對病毒或細胞有害。因此，限制了差錯經由群體的傳播。譬如，諸多突變會調整，於DNA或RNA中，被編碼之蛋白質的構材。這會改變蛋白質的最終形狀，而阻止其達成預期的作用。
“It doesn’t make the nice little curlicue alpha-helices it’s supposed to,” she says of a common structure found in proteins. “It doesn’t make the nice folded sheets it's supposed to.”
她宣稱:「它不會產生其應該是適切之小旋渦狀的α-螺旋(這是於蛋白質中，被發現的一種常見結構)，它沒有產生應有之適切折疊的片段。」
Many other mutations are neutral, having no effect on how efficiently a virus or cell reproduces. Such mutations sometimes spread at random, when a virus carrying the mutation spreads to a population that hasn’t been exposed to any variants of the virus yet. “It’s the only kid on the block,” Anthony says.
諸多其他突變是中性的，對病毒或細胞繁殖的效率沒有影響。當具有突變的病毒傳播到，尚未曾被曝露於任何變異體的群體時，此類突變有時會隨機傳播。Anthony宣稱:「這是進行中，最佳的新突變。」
However, a select few mutations prove useful to a virus or cell. For example, some changes could make a virus better at jumping from one host to the next, helping it outcompete other variants in the area.
不過，少數極佳的突變證實，對病毒或細胞是有益的。譬如，一些改變可能使病毒善於，從一個宿主跳躍到下一個宿主。從而在此領域，協助其從其他諸多變異體勝出。
This was what happened with the SARS-CoV-2 variant B.1.1.7 that was first identified in the United Kingdom but has now spread to dozens of countries around the world. Scientists estimate the variant is roughly 50 percent more transmissible than past forms of the virus, giving it an evolutionary edge.
這是最早在英國被確認，不過現在已經傳播到全球數十個國家之SARS-CoV-2變異體，B.1.1.7所發生的情況。科學家們估計，這種變異體比過去的病毒形式，更可傳播約略50%。這賦予其一種演化優勢。
Mutations may happen randomly, but the rate at which they occur depends on the virus. The enzymes that copy DNA viruses, called DNA polymerases, can proofread and fix errors in the resulting strings of genetic letters, leaving few mutations in each generation of copies.
諸多突變可能隨機發生，不過發生的速度取決於病毒。被稱為DNA聚合酶之複製DNA病毒的酵素，在從而產生之遺傳鹼基串中，能校對及修復錯誤，而在每一代複製物中，留下很少的突變。
But RNA viruses, like SARS-CoV-2, are the evolutionary gamblers of the microscopic world. The RNA polymerase that copies the virus’s genes generally lacks proofreading skills, which makes RNA viruses prone to high mutation rates—up to a million times greater than the DNA-containing cells of their hosts.
不過，如同SARS-CoV-2，RNA病毒是微觀世界的演化賭徒。複製該病毒基因的RNA聚合酶，通常缺乏校對能耐。這使得RNA病毒易發生高突變率——比其宿主具有DNA的細胞，更高達一百萬倍。
Coronaviruses have a slightly lower mutation rate than many other RNA viruses because they can do some light genetic proofreading.“But it’s not enough that it prevents these mutations from accumulating,”says virologist Louis Mansky, the director for the Institute for Molecular Virology at the University of Minnesota. So as the novel coronavirus ran amok around the world, it was inevitable that a range of variants would arise.
冠狀病毒具有比諸多其他RNA病毒，稍低的突變率。因為，它們能進行一些輕微的基因校對。病毒學家Louis Mansky(美國明尼蘇達大學，分子病毒學研究所所長)宣稱:「不過，這阻止此些突變積累，是不夠的。」 因此，隨著新型冠狀病毒，在世界各地肆虐，難免會出現一系列變異體。
The true mutation rate of a virus is difficult to measure though. “Most of those mutations are going to be lethal to the virus, and you’ll never see them in the actively growing, evolving virus population,” Mansky says.
雖然，病毒的真正突變率很難測量。Mansky宣稱:「大多數的此些突變，對此病毒會是致命的。因此，在活躍進行增長、演化的病毒種群中，絕不會發現它們。」
Instead, genetic surveys of sick people can help determine what’s known as the fixation rate, which is a measure of how often accumulated mutations become “fixed” within a viral population. Unlike mutation rate, this is measured over a period of time. So the more a virus spreads, the more opportunities it has to replicate, the higher its fixation rate will be, and the more the virus will evolve, Duffy says.
因此，病人的基因調查能有助於確定，所謂的固定率。這是衡量病毒種群中，累積的突變多久成為“固定的”一種標準。不同於突變率，這是在一段時間內測量的。Duffy表示，因此病毒傳播越多，其必需複製的機會越多。其固定率會是較高，因此病毒會演化越多。
For SARS-CoV-2, scientists estimate that one mutation becomes established in the population every 11 days or so. But this process may not always happen at a steady pace.
就SARS-CoV-2而言，科學家們估計，在此種群中，經證實每11天左右，出現一個突變。不過，此過程不可能總是，以穩定的步調發生。
In December 2020, the variant B.1.1.7 caught scientists’attention when its 23 mutations seemed to suddenly crop up as the virus rampaged through Kent, England.
於2020 年 12 月，隨著病毒在英國肯特郡肆虐，變異體B.1.1.7似乎突然出現其23個突變時，引起了科學家們的注意。
Some scientists speculate that a chronically ill patient provided more opportunities for replication and mutation, and the use of therapies such as convalescent plasma may have pressured the virus to evolve. Not every change was necessarily useful to the virus, Duffy notes, yet some mutations that emerged allowed the variant to spread rapidly.
一些科學家推測，慢性病患者提供了，更多複製及突變的機會，及諸如使用康復期血漿等療法，可能已經迫使病毒演化。Duffy特別指出，並非每一改變對病毒必然有益。不過，出現的某些突變，使該變異體得以迅速傳播。
Mutations drive evolution, but they are not the only way that a virus can change over time. Some viruses, like influenza, have other ways to increase their diversity.
諸多突變驅動演化，不過它們並非病毒，隨著時間推移，能會改變的唯一方式。如同流感，某些病毒有其他方法，來增加其多樣性。
Influenza is made up of eight genetic segments, which can be rearranged—a process called reassortment—if multiple viruses infect a single cell to replicate at the same time.
流感由八個基因片段組成，倘若多個病毒同時感染單個細胞來進行複製，這些片段會被重新排列。
As the viral progeny are packaged into their protein capsules, the RNA segments from the parent viruses can be mixed and matched like viral Legos. This process can cause rapid shifts in the viral function. For example, reassortments of flu strains circulating in pigs, birds, and humans led to the 2009 H1N1 flu pandemic.
這是一種，被稱為重配的過程。當病毒後代被封包進入其蛋白質膠囊中時，來自母病毒的RNA片段，會如同病毒樂高積木一樣，被混合及相配。此過程會導致病毒功能快速變化。譬如，在豬、鳥類及人類中，傳播之流感病毒株的重配，導致了2009年H1N1流感的大流行。
The influenza virus is a recurring nightmare, killing thousands of people each year. Learn how the virus attacks its host, why it's nearly impossible to eradicate, and what scientists are doing to combat it.
流感病毒是一種反復出現的夢魘，每年造成數千人死亡。瞭解病毒如何攻擊其宿主，為何幾乎不可能根除，及科學家們正進行什麼，來對抗它。
Unlike influenza, however, coronaviruses possess no physical segmentation to undergo reassortment. Coronaviruses can experience some shifts in function through a process known as recombination, when segments of one viral genome are spliced onto another by the enzyme making the viral copy. But researchers are still working to determine how important this process is for SARS-CoV-2’s evolution.
不過，不同於流感，冠狀病毒不具有進行重配的物理分割。當一個病毒基因體的諸片段，被產生病毒複製物的酵素，拼接到另一病毒基因體時，冠狀病毒經由一種，被稱為重組的過程，會經歷功能上的一些變化。不過，研究人員仍致力於，確定此過程對SARS-CoV-2的演化，是多重要。
Understanding these evolutionary dynamics of SARS-CoV-2 is vital to ensure that treatments and vaccines keep pace with the virus. For now, the available vaccines are effective in preventing severe disease from all the viral variants.
瞭解SARS-CoV-2的此些演化動態，對確保治療及疫苗與病毒保持同步，是至關重要的。在預防所有該病毒變異體引起的嚴重疾病上，就目前可資使用的疫苗而言，是有效的。
And the study of SARS-CoV-2’s evolution could help answer another looming question: Where did the virus come from? While the disease likely originated from bats, there are still missing chapters in the tale of SARS-CoV-2’s leap to human hosts. Filling in these blanks could help us learn how to protect ourselves in the future.
因此，SARS-CoV-2的演化研究，可能有助於回答另一項迫切問題：病毒從何而來？雖然這種疾病可能源自蝙蝠，不過在SARS-CoV-2跳躍到人類宿主的故事中，仍然缺少諸多章節。填補這些空白可能有助於，人們得悉於未來，如何保護咱們自己。
網址：https://www.nationalgeographic.com/science/article/the-coronavirus-is-mutating-but-what-determines-how-quickly
翻譯: 許東榮
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