Goutam Das doesn’t remember much about his five weeks in intensive care with COVID-19.

Mainly the nightmares, and struggling to breathe.

“It’s almost like if somebody puts you underwater. It’s that kind of feeling… you’re just desperate for oxygen.”

He’s now back at work and putting his ordeal behind him. But while he was in the ICU, Goutam did not suffer entirely in vain.

He’s one of the thousands of people who became severely ill with COVID who gave a sample of their DNA to researchers based at the University of Edinburgh.

It’s now become a genetic resource that could be a goldmine for discovering new drugs – not just to treat COVID – but other forms of severe lung inflammation, one of the leading causes of death in intensive care.

While the pandemic was still at its height, the team in Edinburgh led by Prof Kenneth Baillie, used genetic insights gained from severely ill patients like Goutam to show that the arthritis drug Baracitinib would help treat the severe lung inflammation.

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“In infectious disease and intensive care medicine, to my knowledge, this is the first time that we’ve been able to go from a genetic discovery straight to a drug,” Prof Baillie tells me.

The results formed part of the GenOMICC study which has identified more than 16 genetic changes that underpin the severe lung inflammation that killed many of those who died from COVID-19.

Crucially, the same syndrome also causes death from commonly lethal conditions like sepsis, acute respiratory distress syndrome (ARDS) and pneumonia.

Now Prof Baillie and his team have been given £15m from Scottish investment firm Baillie Gifford (no relation to the Prof) to turn more of their genetic insights into new drugs to tackle those conditions.

A new Pandemic Science Hub at the University brings the disciplines they used to make their initial drug breakthrough under one roof: human genetics to identify new drug targets based on genetic signals found in critically ill patients; a drug manufacturing facility to make experimental drugs based on those targets, and a technology team to design better ways of screening those drugs in patients.

And it’s with Prof Kev Dhaliwal, who leads that team, that I find myself watching a donated human lung breathe again.

The deepest part of the human lung, where oxygen from the air we breathe dissolves into the blood is “like a black hole,” he tells me. “It’s a bit like the outer cosmos where we don’t really know what’s going on.”

For that reason, even the most promising drugs identified using a patient’s genetics, may not behave how they expect once they reach their intended target deep in the lung tissue.

The experimental setup we’re looking at is designed to overcome that hurdle.

The donated lung, from an ex-smoker that isn’t suitable for donation, is being filled with air by a ventilator.

A robotic arm is then taught to pass an ultrafine fibre optic microscope deep into the lung. A parallel tube allows the researchers to place their experimental medicine in a precise spot.

Using the robot allows them to inject multiple different drugs, in tiny doses, into the same lung and then return to those same locations to see if the drug is having the desired effect.

The next step, once the robot has been optimised on donated lungs, is to take their robotic technology into the hospital and use it to screen their experimental drugs on patients with severe lung inflammation.

“We can lead optimise, we can choose which ones to take forward or pass on to other trial systems,” says Prof Dhaliwal.

“That allows us to do this in small numbers of patients and get answers very quickly.”

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