Continued from yesterday
Zania Stamataki – The Goldilocks principle applies here: if the mutations are too subtle, the viral coat will be easily identified by existing antibodies, whereas if they are too drastic they might simply inactivate the virus.
The mutations that allow viruses to fly under the radar fall somewhere in between. Influenza viruses, which use rapidly evolving ribonucleic acid (RNA) as their genetic material, are experts at this game.
History teaches us that influenza mutations can result in pandemics with millions of deaths, so we’ve learned to keep a watchful eye on them.
As flu evolves over the months, virologists respond by producing seasonal vaccines that remain effective — for a time, at least.
Coronaviruses have RNA genomes too, but they are very large.
That means that there are many more opportunities for mutations to go wrong – from the virus’s point of view.
As a result, they have developed a sort of “proof-reading” mechanism that edits out mutations –— meaning that they change a lot less rapidly than flu does.
This is good news for us, and for vaccine development. But we still need more information to determine just how long a vaccine might be effective for.
How does a virus go on to achieve world domination? Getting from A to B is of the essence.
Sars-Cov-2 rides droplets propelled by coughs and sneezes to board a new host.
This is a more effective route of transmission than that used by non-respiratory viruses like Ebola, and its efficiency is increased if the virus particles are more stable and can survive on surfaces outside the body.
This is why keeping a safe distance from each other and isolating patients is so useful in preventing new infections.
Sars-Cov-2 also has a lipid-containing coat, so thorough handwashing with soap, which breaks down fats, can stop it in its tracks.
It should be increasingly clear that to end the pandemic and keep Covid-19 outbreaks to a minimum, we need to seriously upgrade our spyware.
We need surveillance teams of epidemiologists that decipher patterns of viral spread and molecular virologists to track virus evolution so we can update our defences.
We need immunologists to help to understand how the body fights the virus and aid vaccine research.
We also need trained and well-equipped doctors and nurses to safely look after infected people, and scientists to help design effective treatments.
We need to fund these heroes well, and keep their kit up to date, and we need structures and public health strategies in place to promote hygiene, contain outbreaks and prevent transmission.
Covid-19 has shown us that we must stay vigilant, and each of us can personally help break the transmission cycle.
What if a new pathogen emerges and bears all those terrifying hallmarks of viral success –— it doesn’t kill us quickly, mutates often, and is easily transmitted? We rely on the World Health Organisation to report new outbreaks and international teams of experts to act rapidly to contain them.
It’s important that both receive proper funding and support from governments.
When someone like Newman, or the UK’s Public Health Rapid Support Team, receives a call to pick up their pop-up lab and join other defenders at the heart of the outbreak, not everyone welcomes them on location, and people are understandably reluctant to keep away from their infected loved ones.
These teams will have their work cut out for them. But their work is vital.
And when they return they will doubtless have lots of stories to share with the new generation of virologists — some of them, hopefully, inspired to join the fight by the crisis we’re now battling.
Stamataki is a senior lecturer and researcher in viral immunology at the University of Birmingham