“This is the revenge of the viruses,” said Dr. Peter Piot, the director of the London School of Hygiene and Tropical Medicine. “I’ve made their lives difficult. Now they’re trying to get me.”
“A week ago, I couldn’t have done this interview,” he said, speaking recently by Skype from his London dining room, a painting of calla lilies behind him. “I was still short of breath after 10 minutes.”
Looking back, ruefully, on being brought down by a virus after a life as a virus hunter, Piot said he had misjudged his prey and had become the hunted.
“I underestimated this one — how fast it would spread,” he said. “My mistake was to think it was like SARS, which was pretty limited in scope. Or that it was like influenza. But it’s neither.”
In 1976, as a graduate student in virology at the Institute of Tropical Medicine in Antwerp, Belgium, Piot was part of the international team that investigated a mysterious viral hemorrhagic fever in Yambuku, Zaire, now the Democratic Republic of Congo.
To avoid stigmatizing the town, team members named the virus “Ebola” after a nearby river.
Later, in the 1980s, he was one of the scientists who proved that the wasting disease known as “slim” in Africa was caused by the same virus that was killing young gay men elsewhere.
From 1991 to 1994, he was president of the International AIDS Society, and then the first director of UNAIDS, the United Nations’ anti-HIV program.
That expertise made him keenly alert to the danger posed by the new coronavirus. In late January, he and his wife, Heidi Larson, an anthropologist, went to a medical conference in Singapore, which had had its first case a week earlier. While there, he gave an impromptu interview to local television on the day the World Health Organization declared the emerging virus a public health emergency of international concern.
“We started banning handshaking from our behavior,” he said. “We went out to eat because we like good food, but we started giving the ‘Ebola elbow.’”
In early March, he went to Boston with Larson, who heads the Vaccine Confidence Project at the London School of Hygiene and Tropical Medicine. She gave a TedMed talk about rumors that damage vaccination campaigns, and he was asked 100 questions about the virus.
No. 79: “Should I be worried that I’m going to get COVID-19? How worried are you, Peter?”
He advised, “I would do everything I can to avoid becoming infected as you don’t know individual outcomes.”
He became a living illustration of that.
Although medical conferences in the Boston area that week were turning into superspreader events, Piot almost undoubtedly did not get infected there.
Back home in London, he spoke to audiences of 30 to 250, attended a 50-person birthday party and had dinner or drinks in five restaurants in London or Cambridge.
“My usual modus operandi,” he said. Aside from avoiding handshakes, he took no particular precautions. “I really don’t know where I was infected.”
Although there were then already many confirmed cases, Britain did not officially go into lockdown until March 23, when there were 335 confirmed deaths. Piot and his wife, by contrast, began working from home on March 16.
The evening of March 19, he began feeling feverish and developed a headache.
“My immediate thought was, ‘Oh, I hope it’s not COVID.’”
Each day he felt more tired, his fever hovering around 100 degrees.
“It hit me like a bus,” he said. “Extreme exhaustion, like every cell in your body is tired. And my scalp was very sensitive — it hurt if Heidi touched it. That’s a neurological symptom.”
It was a new feeling. Despite all the time he has spent in mosquito-riddled climes, “I’d never been seriously ill in my life,” he said. A regular jogger and apparently healthy, he joked, “This is the first time in my adult life I didn’t drink wine for a month.”
Larson, on the other hand, has survived a fusillade of tropical diseases in her travels: cerebral malaria, hepatitis E, typhoid and dengue.
“I knew how a lot of the symptoms Peter had felt — how you hold your head when it hurts, how fatigued you get just moving across the room,” she said. “So if he asked for water, or anything, I dropped what I was doing and got it immediately. Time is a different experience when you’re not well — every minute matters.”
At the time, it was almost impossible to get tested; the few kits available were reserved for hospitals.
On March 26, Piot finally found a kit through a private doctor. It was positive, and his fever kept rising.
On March 31, it hit 104 degrees and he began feeling confused. He and his wife went to the emergency room of St. Bartholomew’s Hospital. Although he did not feel short of breath, his oxygen saturation was only 84%, dangerously low. An X-ray showed fluid in both lungs in a pattern that suggested bacterial pneumonia.
His blood tests “were really bad,” he said. His levels of C-reactive protein, which indicate inflammation, and of D-Dimer, which indicate blood clots forming, were both very high.
“I instantly changed from doctor to patient,” he said. He was put on oxygen and sent upstairs on a gurney.
“That was when it hit me in the stomach,” Larson said. She had been allowed to stay while he was assessed but could not venture upstairs.
Normally, Britain’s National Health Service hospitals “are as crowded as Indian buses,” Larson said. “But they had a campaign saying, ‘Don’t come to the hospital unless you’re in the eleventh hour,’ so it was almost empty.”
She continued: “But when I saw Peter go through the double doors on that cart — I had the same feeling as the Ebola families we knew in Sierra Leone: They were hiding their relatives because they didn’t want to be separated from them emotionally, knowing they might never see them again.”
At first, Piot said, he was so exhausted he was apathetic. He asked for a single room but was told they were reserved for people who had not tested positive, for their protection. He was put in a 20-by-22-foot room, one bathroom, with three other men.
“They call the NHS ‘the great equalizer,’” he said. “The food was bangers and mash — awful.”
He got intravenous antibiotics and high-flow oxygen, and was roused every two hours for checks on his blood pressure and other vital signs.
“I was particularly anxious that I not be put on a ventilator,” he said. “Ventilators can save lives, but they can also do a lot of harm. Once you’re on one, your chances of surviving are the same as of surviving Ebola — about one-third.”
Every day, he talked to Larson or his grown children. He did get to watch episodes of a new BBC series about a Sicilian detective, “Inspector Montalbano,” that his wife recommended.
“If this had happened before cellphones, can you imagine the loneliness?” he said. “It’s like being in prison. Look, I know I’m privileged, and I know I’m not going to be stuck here for 27 years like Nelson Mandela. But the world shrinks to the essentials. All you can think is, ‘How is my breathing going?’”
Finally, Piot said, his oxygen saturation came up to 92%. He was discharged on April 8.
But his body wasn’t through with the disease.
Before the hospital released him, he had tested negative for the virus. But now something else was going on — a delayed immune reaction.
“Gradually, I became short of breath,” he said. “We live in an old Georgian house, with three floors, and I had a hard time getting upstairs.”
Larson bought a pulse oximeter, a fingertip monitor that measures blood oxygen levels.
She recently tested positive for antibodies to the virus herself, although her illness was so mild that she’s not sure when it peaked. She had two bouts of bad headaches, the first in late March and the second in mid-April. The second time, she also had itchy red eyes, which are a rare but recognized symptom and may indicate infection through the eyes.
On April 15, Piot’s heart started to race to 165 beats a minute. The percentage of his blood oxygen dropped to the mid-80s again.
He and Larson went to the University College Hospital, where he had a chest X-ray.
This time, instead of distinct bacterial masses on each side, “my lungs were full of infiltrates, and they were a real mess,” he said, adding, “It’s called ‘organizing pneumonia.’”
The tiny sacs that grow like bunches of grapes throughout the lungs, he explained, were oozing signaling proteins — he was having a “cytokine storm.” Those drew voracious white blood cells into the spaces between the air sacs so they threatened to block the paths oxygen normally takes to his red blood cells.
His doctors thought about rehospitalizing him — an outcome he dreaded.
Instead, Dr. Joanna Porter, who specializes in difficult pneumonias, put him on an intravenous steroid to reduce the inflammation, along with an anticoagulant to prevent blood clots from his atrial fibrillation.
Britain’s NHS bureaucracy forbade her from discussing Piot’s treatment, though he gave his permission. He is still under her care.
Last week, a PET scan, CT scan and bronchoscopy showed that parts of his lungs had not completely cleared. “And,” he added, ever the universal health care booster, “tell your American audience: All these expensive tests are free from the NHS.”
The steroids appear to be working, but taking them for too long can have side effects, including muscle wasting, weakening of bones and diabetes.
He may have to take anticoagulants for the rest of his life, he said, and parts of his lungs may permanently be scarred.
“But you can live with that,” he added, shrugging.
“If you get this cytokine storm while you’re acutely ill, you’re finished,” he said. “But I had three stages — first fever, then needing oxygen, and now the storm.
“People think that with COVID-19, 1% die and the rest just have flu. It’s not that simple — there’s this whole thing in the middle.”
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