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Cuts off oxygen to organs.
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Hi, it’s Jason in Melbourne. Covid-19 might just be the disease that keeps on giving. Before I explain ... 

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Today’s must-reads

  • Trump is downplaying the effects of Medicaid cuts in the tax bill. 
  • Canadian wildfire smoke worsens air quality in the US Northeast. 
  • Women who work at Novo Nordisk are paid more on average than the men. 

Bursting blood cells

More than five years after the coronavirus stormed into our lives, scientists are still piecing together why it was so deadly — and why it’s left millions with lingering illness.

Early on, doctors noticed unusual blood clots in Covid patients and used blood thinners in severe cases. Later, researchers in San Francisco showed that the virus’s spike protein could stick to clotting agents and create clumps of inflammation-inducing fibrin — a protein involved in healing wounds.

Now, new research reveals another, and no less insidious, form of damage.

In a study just published in Nature, Australian scientists found that when oxygen-rich blood can’t reach tissues, the delicate lining of blood vessels starts to break down. The death of these endothelial cells, which Covid can trigger, sets off immune signals that cause red blood cells to burst, spilling their sticky contents into the bloodstream.

“This stuff’s like glue,” says Sydney-based hematologist Shaun Jackson, who led the study. It clogs the tiniest blood vessels, blocking circulation. 

The damage builds. Without oxygen and nutrients, tissues begin to fail, potentially affecting organs like the kidneys, liver and heart.

“It’s a double whammy,” Jackson says.

When his team analyzed more than 1,000 samples from Covid patients, they expected to see widespread fibrin and clotting. But they didn’t.

“To our great surprise, that wasn’t the case at all,” he says. While large vessels showed some clots, the smallest capillaries — just a fraction the width of a hair — were clogged not with clots, but with debris from broken red blood cells.

“No one had thought it was through this dying endothelial cell mechanism,” Jackson says. “It was by far and away the biggest issue going on in the microcirculation.”

Past studies have shown that sicker Covid patients had worse capillary damage. Now, researchers are spotting similar patterns in patients with long Covid, which may help explain the lingering symptoms.

Stopping the death of these vessel-lining cells could help prevent the whole cascade, Jackson says, though it would likely take a mix of treatments.

These findings could also change how we understand what happens in stroke, heart attack and other serious conditions — especially when patients don’t improve with standard care.

“This study represents a significant leap forward in our understanding of how Covid wreaks havoc in the body,” said Ziyad Al-Aly, a clinical epidemiologist at the Veterans Affairs St. Louis Health Care System, who’s studied Covid’s long-term impacts. 

With this new insight, scientists may be able to develop treatments to help patients recover, not just during a Covid infection, but long after it ends. — Jason Gale

What we’re reading

The New York Times breaks down the NIH grants that have been ended or delayed in this data visualization.

The FDA’s AI tool is struggling with simple tasks, NBC News reports

Ultra-processed foods are attractive in part because of their textures, the Wall Street Journal reports.

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