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How the new coronavirus attacks the brain



The coronavirus targets mainly the lungs, but also the kidneys, liver and blood vessels. However, about half of patients report neurological symptoms, including headache, confusion, and delirium, suggesting that the virus may also attack the brain.

A new study offers the first clear evidence that in some people, the coronavirus invades brain cells, abducting them to make copies of itself. The virus appears to suck in all the oxygen nearby, starving neighboring cells to death.

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It is not clear how the virus reaches the brain or how often it travels this path of destruction. Brain infections are likely to be rare, but some people may be susceptible due to their genetic background, high viral load, or other causes.

“If the brain becomes infected, it can be fatal,”

; said Akiko Iwasaki, an immunologist at Yale University who oversees the work.

The study was published online on Wednesday and has not yet been verified by experts for publication. But several researchers have said it is careful and elegant, showing in many ways that the virus can infect brain cells.

The researchers had to rely on brain images and patients’ symptoms to infer the effects on the brain, but “we didn’t actually see much evidence that the virus could infect the brain, although we knew it was a potential possibility,” he said. Dr. Michael Zandi, consultant neurologist at the National Hospital of Neurology and Neurosurgery in the UK. “These data just provide a little more evidence that they certainly can.”

Zandi and colleagues published a study in July that showed that some patients with Covid-19, a disease caused by the coronavirus, developed serious neurological complications, including nerve damage.

In the new study, Iwasaki and colleagues documented a brain infection in three ways: in the brain tissue of a man who died of Covid-19, in a mouse model, and in organelles, clusters of brain cells in a laboratory dish designed to mimic the three-dimensional structure of the brain.

Other pathogens – including the Zika virus – are known to infect brain cells. Immune cells then flood the damaged areas, trying to clear the brain by destroying the infected cells.

The coronavirus is much more stolen: it uses the mechanism of brain cells to multiply, but does not destroy them. Instead, it suffocates the oxygen in neighboring cells, causing them to dry out and die.

The researchers found no evidence of an immune response to eliminate this problem. “It’s kind of like a silent infection,” Iwasaki said. “This virus has many mechanisms to avoid.”

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These findings are consistent with other observations of coronavirus-infected organelles, said Alison Muotri, a neurologist at the University of California, San Diego, who also studied the Zika virus.

The coronavirus appears to rapidly reduce the number of synapses, the connections between neurons.

“Days after the infection, we are already seeing a drastic reduction in the number of synapses,” Muotri said. “We still don’t know if this is reversible or not.”

The virus infects a cell through a protein on the surface called ACE2. This protein appears in the body and especially in the lungs, explaining why they are the preferred targets of the virus.

Previous studies have suggested, based on a proxy for protein levels, that the brain has very little ACE2 and is likely to be spared. But Iwasaki and her colleagues looked more closely and found that the virus could indeed enter brain cells using this door.

“Clearly, it’s expressed in neurons and is needed to enter,” Iwasaki said.

Her team then examined two sets of mice, one with an ACE2 receptor expressed only in the brain and the other with the receptor only in the lungs. When the virus was introduced into these mice, the brain-infected mice quickly lost weight and died within six days. Lung-infected mice did neither.

Despite warnings from mouse studies, the results still suggest that a viral infection in the brain could be more deadly than a respiratory infection, Iwasaki said.

The virus can reach the brain through the olfactory bulb – which regulates odor – through the eyes or even from the bloodstream. It is not clear which path the pathogen travels and whether it does so often to explain the symptoms seen in humans.

“I think this is a case where scientific data is ahead of clinical evidence,” Muotri said.

Researchers will need to analyze many autopsy samples to assess how common the brain infection is and whether it is present in people with a mild illness or in so-called long carriers, many of whom have multiple neurological symptoms.

Forty percent to 60 percent of patients with Covid-19 experience neurological and psychiatric symptoms, said Dr. Robert Stevens, a neurologist at Johns Hopkins University. But the symptoms may not be due to the virus invading the brain cells. They can be the result of widespread inflammation throughout the body.

For example, inflammation in the lungs can release molecules that make the blood sticky and clog blood vessels, leading to strokes. “There is no need for the brain cells themselves to be infected for this to happen,” Zandi said.

But some people, he added, may have low levels of oxygen in their blood from infected brain cells, causing strokes: “Different groups of patients can be affected differently,” he said. “It’s entirely possible to see a combination of both.”

Some cognitive symptoms, such as brain fog and delirium, may be more difficult to perceive in patients who are sedated and on ventilators. Doctors should plan to take sedatives once a day, if possible, to evaluate patients with Covid-19, Stevens said.


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