For all its huge genome and clever tricks, Sars-CoV-2 has significant vulnerabilities. It has a fairly feeble fatty envelope, which it needs to sneak into cells. That’s destroyed by soap, and by alcohol – so washing your hands carefully or smearing them in alcohol hand gel will kill the virus. Most transmission is either by very close contact – someone coughs or sneezes in your face – or because a droplet containing the virus touches your hands, and then you touch your face; the virus gets into the body especially easily through the membranes in the eyes, nose and mouth. Expect to be bored to tears over the coming months by pious injunctions to wash your hands. It doesn’t seem like much, but it’s going to reduce the risk at least somewhat.

The second great vulnerability of the virus is that it has to take great pains copying its genome. All RNA viruses (influenza, for example) have a special enzyme that copies RNA into RNA. These RNA-dependent RNA polymerases are usually very sloppy copyists. They do not bother with proofreading, and make huge numbers of errors. This high mutation rate enables them to evolve very rapidly; that’s one reason we need a new flu vaccine every year. Coronaviruses have to be much more careful, or else their huge genome will accumulate too many errors. Their mutation rate is therefore lower, so we may be able to develop a fairly effective vaccine – though it will take a year or two, assuming it’s possible at all.

We can also target the virus with drugs. Remdesivir was developed to target the Ebola polymerase, and may also work against Sars-CoV-2. It certainly works in a Petri dish, and there are ongoing clinical trials in China and the US to see if it works in humans. Sars-CoV-2 produces many of its genes in long, multi-functional proteins that need to be chopped up – by its own ‘protease’ enzymes – into the right chunks. Such proteases have been successfully targeted by antiviral drugs in viruses like Hepatitis C. In my lab we are trying to work out which human proteins Sars-CoV-2 needs to replicate, and the interactions between virus and host may also be good drug targets. But we are a long way off, so in the meantime, what should we do?

I received an email from a colleague in infectious diseases. His message was in no way reassuring. He made three main points:

1. This is not business as usual. This will be different from what anyone living has ever experienced. The closest comparator is 1918 influenza.

2. early social distancing is the best weapon we have to combat Covid-19.

3. Humanity will get through this fine, but be prepared for major changes in how we function and behave as a society until either we’re through the pandemic or we have mass immunisation available.

I am writing in haste. This is a fast-moving situation, and the numbers are constantly changing – certainly the ones I have given here will be out of date by the time you read this. What’s very clear is that we must comply immediately with whatever measures competent public health authorities urge us to take, even if they seem disproportionate. It’s time to increase ‘social distance’ in all sorts of ways. And wash your hands.
https://www.lrb.co.uk/the-paper/v42/n06/rupert-beale/short-cuts
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