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Introduction:
SARS-CoV-2 Delta variant, also known as lineage B.1.617.2, or Indian variant is a variant of lineage B.1.617 of SARS-CoV-2, the virus that causes COVID-19. It was first detected in India in late 2020. The World Health Organization named it the Delta variant on 31 May 2021.
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ANALYSIS:
The Covid-19 pandemic is a dramatic demonstration of evolution in action. Evolutionary theory explains much of what has already happened, predicts what will happen in the future and suggests which management strategies are likely to be the most effective.
For instance, evolution explains why the Delta variant spreads faster than the original Wuhan strain. It explains what we might see with future variants. And it suggests how we might step up public health measures to respond.
But Delta is not the end of the story for SARS-CoV-2, the virus that causes Covid-19. Here's what evolutionary theory tells us happens next.
Remind me again, how do viruses evolve?
Evolution is a result of random mutations (or errors) in the viral genome when it replicates. A few of these random mutations will be good for the virus, conferring some advantage. Copies of these advantageous genes are more likely to survive into the next generation, via the process of natural selection.
New viral strains can also develop via recombination, when viruses acquire genes from other viruses or even from their hosts.
Generally speaking, we can expect evolution to favour virus strains that result in a steeper epidemic curve, producing more cases more quickly, leading to two predictions.
First, the virus should become more transmissible. One infected person will be likely to infect more people; future versions of the virus will have a higher reproductive or R number.
Second, we can also expect evolution will shorten the time it takes between someone becoming infected and infecting others (a shorter "serial interval").
Both these predicted changes are clearly good news for the virus, but not for its host.
Aha, so that explains Delta
This theory explains why Delta is now sweeping the world and replacing the original Wuhan strain.
The original Wuhan strain had an R value of 2-3, but Delta's R value is about 5-6 (some researchers say this figure is even higher). So someone infected with Delta is likely to infect at least twice as many people as the original Wuhan strain.
There's also evidence Delta has a much shorter serial interval compared with the original Wuhan strain.
This may be related to a higher viral load (more copies of the virus) in someone infected with Delta compared with earlier strains. This may allow Delta to transmit sooner after infection.
A higher viral load may also make Delta transmit more easily in the open air and after "fleeting contact".
Do vaccines affect how the virus evolves?
We know Covid-19 vaccines designed to protect against the original Wuhan strain work against Delta but are less effective. Evolutionary theory predicts this; viral variants that can evade vaccines have an evolutionary advantage.
So we can expect an arms race between vaccine developers and the virus, with vaccines trying to play catch up with viral evolution. This is why we're likely to see us having regular booster shots, designed to overcome these new variants, just like we see with flu booster shots.
Covid-19 vaccines reduce your chance of transmitting the virus to others, but they don't totally block transmission. And evolutionary theory gives us a cautionary tale.
There's a trade-off between transmissibility and how sick a person gets (virulence) with most disease-causing microorganisms. This is because you need a certain viral load to be able to transmit.
If vaccines are not 100 per cent effective in blocking transmission, we can expect a shift in the trade-off towards higher virulence. In other words, a side-effect of the virus being able to transmit from vaccinated people is, over time, the theory predicts it will become more harmful to unvaccinated people.
How about future variants?
In the short term, it's highly likely evolution will continue to "fine tune" the virus:
• its R value will continue to increase (more people will be infected in one generation);
• the serial interval will decrease (people will become infectious sooner);
• variants will make vaccines less effective (vaccine evasion).
But we don't know how far these changes might go and how fast this might happen.
Some scientists think the virus may already be approaching "peak fitness". Nevertheless, it may still have some tricks up its sleeve.
The UK government's Scientific Advisory Group for Emergencies (SAGE) has recently explored scenarios for long-term evolution of the virus.
It says it is almost certain there will be "antigenic drift"; accumulation of small mutations leading to the current vaccines becoming less effective, so boosters with modified vaccines will be essential.
It then says more dramatic changes in the virus ("antigenic shift"), which might occur through recombination with other human coronaviruses, is a "realistic possibility". This would require more substantial re-engineering of the vaccines.
SAGE also thinks there is a realistic possibility of a "reverse zoonosis", leading to a virus that may be more pathogenic (harmful) to humans or able to evade existing vaccines. This would be a scenario where SARS-CoV-2 infects animals, before crossing back into humans. We've already seen SARS-CoV-2 infect mink, felines and rodents.
Will the virus become more deadly?
Versions of the virus that make their host very sick (are highly virulent) are generally selected against. This is because people would be more likely to die or be isolated, lowering the chance of the virus transmitting to others.
SAGE thinks this process is unlikely to cause the virus to become less virulent in the short term, but this is a realistic possibility in the long-term. Yet SAGE says there is a realistic possibility more virulent strains might develop via recombination (which other coronaviruses are known to do).
So the answer to this critical question is we really don't know if the virus will become more deadly over time. But we can't expect the virus to magically become harmless.
Will humans evolve to catch up?
Sadly, the answer is no. Humans do not reproduce fast enough, and accumulate enough favourable mutations quickly enough, for us to stay ahead of the virus.
The virus also does not kill most people it infects. And in countries with well-resourced health-care systems, it doesn't kill many people of reproductive age. So there's no "selection pressure" for humans to mutate favourably to stay ahead of the virus.
What about future pandemics?
Finally, evolutionary theory has a warning about future pandemics.
A gene mutation that allows a virus in an obscure and relatively rare species (such as a bat) to gain access to the most common and widely distributed species of large animal on the planet - humans - will be strongly selected for.
So we can expect future pandemics when animal viruses spill over into humans, just as they have done in the past.
Hamish McCallum is director of the Centre for Planetary Health and Food Security at Griffith University in Queensland, Australia.
This article is republished from The Conversation under a Creative Commons license. Read the original article.
Covid 19 冠狀病毒：達美航空將如何發展？這是科學告訴我們的
分析：
Covid-19 大流行是行動中進化的戲劇性展示。進化論解釋了大部分已經發生的事情，預測未來會發生什麼，並建議哪些管理策略可能是最有效的。
例如，進化解釋了為什麼 Delta 變種比原始武漢菌株傳播得更快。它解釋了我們可能會在未來的變體中看到什麼。它建議我們如何加強公共衛生措施來應對。
但是對於導致 Covid-19 的病毒 SARS-CoV-2 而言，Delta 並不是故事的結束。這是進化理論告訴我們接下來會發生的事情。
再次提醒我，病毒是如何進化的？
進化是病毒基因組複製時隨機突變（或錯誤）的結果。這些隨機突變中的一些將對病毒有益，從而帶來一些優勢。通過自然選擇的過程，這些有利基因的副本更有可能存活到下一代。
當病毒從其他病毒甚至宿主身上獲得基因時，新的病毒株也可以通過重組產生。
一般來說，我們可以預期進化有利於導致更陡峭流行曲線的病毒株，更快地產生更多病例，從而導致兩個預測。
首先，病毒應該變得更容易傳播。一名感染者可能會感染更多人；該病毒的未來版本將具有更高的繁殖或 R 值。
其次，我們還可以預期進化將縮短某人被感染和感染他人之間的時間（更短的“連續間隔”）。
這兩種預測的變化顯然對病毒來說都是好消息，但對其宿主卻不是。
啊哈，這就解釋了 Delta
這個理論解釋了為什麼 Delta 現在正在席捲全球並取代原來的武漢菌株。
武漢原株的R值為2-3，而Delta的R值在5-6左右（有研究人員說這個數字更高）。因此，感染三角洲病毒的人感染的人數可能至少是原始武漢病毒株的兩倍。
還有證據表明，與最初的武漢菌株相比，Delta 的序列間隔要短得多。
這可能與感染 Delta 的人比早期毒株更高的病毒載量（更多的病毒拷貝）有關。這可能允許 Delta 在感染後更快地傳播。
更高的病毒載量也可能使 Delta 在露天和“短暫接觸”後更容易傳播。
疫苗會影響病毒的進化方式嗎？
我們知道，旨在抵禦最初的武漢病毒株的 Covid-19 疫苗對 Delta 有效，但效果較差。進化論預測了這一點；可以逃避疫苗的病毒變體具有進化優勢。
因此，我們可以期待疫苗開發者和病毒之間的軍備競賽，疫苗試圖趕上病毒進化。這就是為什麼我們可能會看到我們定期注射加強針，旨在克服這些新變種，就像我們看到的流感加強針一樣。
Covid-19 疫苗可降低您將病毒傳播給他人的機會，但它們並不能完全阻止傳播。進化論給了我們一個警示故事。
在傳染性和一個人對大多數致病微生物的患病程度（毒力）之間存在權衡。這是因為您需要一定的病毒載量才能傳播。
如果疫苗在阻斷傳播方面不是 100% 有效，我們可以預期權衡會轉向更高的毒力。換句話說，該病毒能夠從接種疫苗的人身上傳播的副作用是，隨著時間的推移，該理論預測它對未接種疫苗的人的危害會更大。
未來的變種怎麼樣？
在短期內，進化很可能會繼續“微調”病毒：
• 其R值會不斷增加（一代人會感染更多的人）；
• 序列間隔將減少（人們會更快地具有傳染性）；
• 變異會降低疫苗的效力（逃避疫苗）。
但我們不知道這些變化會走多遠，發生的速度有多快。
一些科學家認為該病毒可能已經接近“健康高峰”。儘管如此，它可能仍然有一些技巧。
英國政府的緊急情況科學諮詢小組 (SAGE) 最近探索了病毒長期進化的情景。
它說幾乎可以肯定會有“抗原漂移”；小突變的積累導致當前疫苗的有效性降低，因此改良疫苗的加強劑將是必不可少的。
然後它說病毒發生更劇烈的變化（“抗原轉變”），這可能是通過與其他人類冠狀病毒的重組而發生的，這是“現實的可能性”。這將需要對疫苗進行更大量的重新設計。
SAGE 還認為存在“反向人畜共患病”的現實可能性，導致病毒可能對人類更具致病性（有害）或能夠逃避現有疫苗。這將是 SARS-CoV-2 感染動物，然後再傳播回人類的情況。我們已經看到 SARS-CoV-2 感染水貂、貓科動物和囓齒動物。
病毒會變得更致命嗎？
通常會選擇使宿主病得很重（毒性很強）的病毒版本。這是因為人們更有可能死亡或被隔離，從而降低了病毒傳播給他人的機會。
SAGE 認為，這個過程在短期內不太可能導致病毒的毒性減弱，但從長遠來看，這是一個現實的可能性。然而，SAGE 表示，通過重組（已知其他冠狀病毒會這樣做），有一種現實的可能性可能會產生更具毒性的菌株。
所以這個關鍵問題的答案是我們真的不知道病毒是否會隨著時間的推移變得更加致命。但是我們不能指望病毒會神奇地變得無害。
人類會進化來追趕嗎？
可悲的是，答案是否定的。人類的繁殖速度不夠快，也不夠快地積累了足夠多的有利突變，無法讓我們領先於病毒。
該病毒也不會殺死它感染的大多數人。在擁有資源豐富的衛生保健系統的國家，它不會殺死許多育齡人群。因此，人類沒有“選擇壓力”來有利地變異以保持領先於病毒。
未來的流行病怎麼辦？
最後，進化論對未來的流行病發出警告。
一種基因突變，允許一種不知名且相對稀有的物種（如蝙蝠）中的病毒接觸到地球上最常見和分佈最廣的大型動物物種——人類——將被強烈選擇。
因此，當動物病毒蔓延到人類身上時，我們可以預見未來的大流行，就像它們過去所做的那樣。
Hamish McCallum 是澳大利亞昆士蘭格里菲斯大學行星健康與食品安全中心主任。
本文根據知識共享許可從 The Conversation 重新發布。閱讀原文。
https://theconversation.com/how-will-delta-evolve-heres-what-the-theory-tells-us-165243
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