How does COVID-19 kill us? Experts warn it can attack more than the lungs

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Understanding how COVID-19 attacks the human body is essential to developing an effective treatment or vaccine to stop the global pandemic – but there is still so much that we do not know how it can kill us.

As researchers around the world rush to understand the disease, they compile and share their first observations of patients affected by a virus that has made more than two million people sick. The results are preliminary, but they can help point the researchers in the right direction.

They saw that in severe cases, COVID-19 invades our respiratory cells and triggers an immune system response that targets these infected cells, destroys lung tissue and ultimately obstructs our airways, cutting off our oxygen supply.

This is when organic failure can also occur, causing serious damage to the kidneys, liver and heart, similar to other infections like sepsis.

But they will seek to determine whether the virus targets and closes organs in a new way or simply behaves like other infections that cause such common complications.

Why COVID-19 can be so deadly

One key thing to understand about coronavirus mortality is how it infects the body and how our body reacts to fight it.

Cytokines are small molecules released by the immune system that move throughout the body to coordinate an immune response against an infection or injury – even with something as mild as a common fever.

But if the immune system overproduces them in response to infection, they can cause “cytokine storms” which can wreak havoc on the bloodstream and seriously damage the body.

Dr. Douglas Fraser, critical care physician at London Health Sciences Center and researcher at Western University in London, Ontario, studied this exaggerated immune response by collecting blood from seriously ill COVID-19 patients to find new ones. ways to treat the disease.

“The immune response to this particular disease is very different from what we have seen in other infected patients who end up in intensive care,” he said. “It is a unique response and it will require unique therapies.”

Fraser said his research shows that there are different types of cytokines released into the body at unusual times and levels in response to COVID-19 compared to those commonly found in critically ill patients with more common diseases.

“What we see seems to happen in all very sick patients: those who need intensive care admissions, those who need help with breathing and those who eventually die,” he said.

Kidneys linked to serious complications

Kidney infection was a “significant complication” in a preliminary publication of a recent observational study out of 287 COVID-19 patients in China, who discovered that nearly one in five patients had a stage of sudden or “acute” kidney infection – putting them at a “significantly higher” risk of death.

While the rate of Canadian COVID-19 patients with acute kidney disease is not yet known, the majority occur in critically ill patients, said Dr. Jeffrey Perl, nephrologist at St Michael’s Hospital in Toronto and assistant professor of medicine at the University of Toronto. .

“As people’s blood pressure gets very low due to a very massive and overwhelming inflammatory immune response, the kidneys are starving for blood,” he said, adding that it can often require a dialysis machine to clean the patient’s blood.

To give an idea of ​​the severity of a complication, Perl said that the mortality rate for patients who had developed acute renal failure from SARS in 2003 was 92%, compared to only 8% for those who did not summer.

Recovery room nurse Maria Tanta, an employee of the Toronto General Hospital, on the left, has her temperature checked by nurse Callie Dunne during the SARS epidemic on April 2, 2003. (J.P. Moczulski / Canadian Press)

Patients with chronic kidney disease are also at higher risk of dying with COVID-19 than those with no pre-existing conditions and who are otherwise healthy, he added.

“We are very concerned that these patients will become infected with COVID-19,” he said. “Like the elderly population of great concern to us, I would consider these patients as another high-risk group.”

Heart can be ‘directly’ targeted by virus

The heart is an essential organ that can be directly exposed to the virus.

A cohort study published in JAMA last month found that almost 20% of the 416 COVID-19 patients hospitalized in China had suffered heart damage while hospitalized, which put them at a higher risk of death.

While recent research from the American College of Cardiology found an arrhythmia, or irregular heartbeat, in 16% of patients and an acute heart injury in 7.2%.

“There is the possibility and the likelihood that part of the virus will directly enter the heart muscle cells and cause this heart damage,” said Dr. Patrick Lawler, cardiologist and clinician scientist at the Peter Munk Cardiac Center in Toronto.

“We hear anecdotes from other people who have had a little more experience, unfortunately, with that which are really compatible with the heart which suddenly begins to become weak.”

An observational study of 187 inpatients with COVID-19 published in the New England Journal of Medicine last month found elevated levels of troponin, which may indicate heart problems, in 28% of COVID-19 inpatients in Wuhan, China, who concluded that they were at risk for “much higher mortality.”

A medical worker checks the condition of a patient at Jinyintan Hospital in Wuhan, central China’s Hubei Province, February 16. New research shows that the heart can be directly threatened by the virus. A study in China found that almost 20% of the 416 patients had heart problems. (Chinatopix / The Associated Press)

Lawler said the results for COVID-19 patients with heart problems are “dramatically worse” and even if the virus enters the respiratory system, it can take root in other parts of the body.

“The heart is really a critical and critical part of what determines whether patients will recover or not,” he said.

Can it help us find a cure?

Lawler is currently studying the use of blood thinners as a possible treatment for patients with COVID-19, which could prevent the virus from binding to ACE2 receivers – enzymes present in the cells of the human body which can serve as a gateway for coronaviruses.

He said research suggests that blood clots may play a role in organ failure in critically ill patients, so different doses of blood thinners can prevent this from happening.

Fraser is also using his research on the “cytokine storm” immune response to COVID-19 to find “targets” to continue efforts towards effective treatment.

He said there could be several elements explaining why different people are susceptible to the virus, ranging from genetics to pre-existing conditions through to age.

“Once we understand what’s going on, we can develop therapies, we can develop vaccines,” he said.

“Then we can go back to normal life.”

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