The Week

Hopes of a cure for Covid

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“The problem with killing coronaviru­s is that it’s already dead,” said Tom Whipple in The Times. Bacteria, by contrast, are complex living systems – they eat, excrete, reproduce; antibiotic­s can work by interferin­g with any of these processes. But a virus is just “a bit of protein mindlessly replicatin­g its way through the world”. And that is why it was big news when, last week, an internatio­nal clinical trial showed that the drug remdesivir had been successful in treating Covid-19 patients. “What did success look like?” Patients taking the drug left hospital four days early – after an average of 11 days, rather than 15 – and “may (or may not)” have had slightly better survival rates. “It was, genuinely, a huge breakthrou­gh.” But it was also, clearly, “no miracle cure”.

Remdesivir, made by the US firm Gilead Sciences, was developed to treat Ebola, said Jennifer Rohn in The Guardian. It didn’t work for that, but it does slow the coronaviru­s by impeding its replicatio­n. It’s one of a range of treatments (as opposed to vaccines) now being trialled, from experiment­al antivirals to “banal substances” such as the heartburn remedy Pepcid and Vitamin C. Covid-19 isn’t just a respirator­y illness, said Harry de Quettevill­e in The Daily Telegraph. “It attacks the heart and kidneys too. Even the brain.” No one knows exactly why. Treating it means treating a series of conditions, as we have learnt to do with HIV. And as with that virus, we may never get a “knockout” cure – but if we develop a range of treatments, in time we will win “on points”.

There is, though, some good news for the here and now, said The Guardian: you probably can’t catch Covid-19 twice. In South Korea, 300 patients had tested positive after recovery, raising the prospect of an endless cycle of infection and reinfectio­n, which would dash all hopes of herd immunity. South Korean scientists have now concluded that those cases were “false positives”.

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