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The writer is a science commentator
Early in the pandemic, scientists were uncertain about how quickly the new coronavirus would mutate. Since then, a steady stream of viral variants has dashed hopes that it might be a slow mover. The Delta variant first identified in India is now the dominant strain in the UK and is spreading rapidly in Europe and the US. Delta is much more transmissible than even the previously fastest-spreading variant although, thankfully, vaccines still appear to be highly effective against it.
It can seem like the onward march of the variants is inevitable and that the virus will mutate to counter our every move. This isn’t necessarily the case. Sars-Cov-2 has proved an unexpectedly fast adversary, but it still has to follow the basic rules of evolution, meaning that its options aren’t limitless.
Evolution occurs when a near-random mutation to the virus’s genetic material becomes a permanent change, often because it benefits the virus in some way, helping it spread faster. Most mutations don’t reach that stage — many even hinder the virus. But when a variant seems to be spreading quickly or behaving differently, scientists begin to worry about the mutations it has.
Sars-Cov-2 variants so far have shown simple changes that allow them to be more infectious, but they haven’t made much headway against natural or vaccine-induced immunity. This probably has to do with natural selection: a faster-spreading virus has a clear advantage. But with only a small fraction of people vaccinated worldwide, there hasn’t yet been much pressure on the virus to evade a trained immune system.
There is a big jump in difficulty between the two tasks. Most of the variants so far have mutations in the spike protein, which protrudes from the body of the virus, its wide end covered in patches that hook on to the surface of our cells, drawing the virus in for infection. One of the main mutations believed to enhance infectivity is D614G, a protein found in the Beta variant first identified in South Africa, which disrupts just a single one of the many bonds that hold the spike together. This probably causes its other components to drift apart slightly, exposing more of the sticky patches that capture our cells. This molecular fine-tuning turbocharges infectiousness.
Taking on the immune system, by contrast, is like fighting a multi-front war. The immune system attacks viruses in many different ways. Neutralising antibodies — human proteins that bind viruses and gum up their machinery, preventing them from finding and fusing with our cells — target multiple sites across the top of the spike protein. One mutation might change one target site enough to flummox the antibody that binds there, but that’s a bit like stopping one bullet in a cannonade.
The virus probably will become better at avoiding our defences, but not all at once. It isn’t just a simple matter of stacking up beneficial mutations — bolting weapon after weapon on to the viral chassis. Evolution is often a process of trade-offs. A recent paper speculated that the Beta variant acquired a mutation that helped it evade some antibodies, but the change cost it some ability to bind human cells.
The evolutionary process is full of these constraints and twisting paths. Evolving to be more infectious may have altered the viral machinery in ways that makes later changes such as immune resistance more difficult. Or there may be yet unknown mutations that allow both improvements to coexist smoothly.
Sars-Cov-2 is probably now the most surveilled genome in history, with tens of thousands of sequences deposited in databases such as the Germany-based GISAID every week. We know an incredible amount. But the modern world has never seen a viral pandemic on this scale. As long as the virus is evolving at this rate, it remains a dangerous, ever-moving target. We will need vigilance and more.