How COVID-19 Kills

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How COVID-19 can kill

April 15th COVID-19 kills by inflaming and clogging the tiny air sacs in the lungs, choking off the body’s oxygen supply until it shuts down the organs essential for life.
But clinicians around the world are seeing evidence that suggests the virus also may be causing:
  • heart inflammation,
  • acute kidney disease,
  • neurological malfunction,
  • blood clots,
  • intestinal damage and
  • liver problems.

The prevalence of these effects is too great to attribute them solely to the “cytokine storm”. This is more like MERS than SARS !

Aggressive and sustained testing gave South Korea 1/7 the Death Rate of Italy ! This includes enforcing a law that grants the S. Korea government wide authority to access data: CCTV footage, GPS tracking data from phones and cars, credit card transactions, immigration entry information, and other personal details of people confirmed to have an infectious disease. The authorities can then make some of this public, so anyone who may have been exposed can get themselves - or their friends and family members - tested.
.....
placed in self-quarantine and monitored remotely through a smartphone app, or checked regularly in telephone calls, until a hospital bed becomes available...
South Korea’s government also uses
location data to customize mass messages sent to cellphones, notifying every resident when and where a nearby case is confirmed.
South Korea changed the law to allow the state to gain access to medical records and share them without a warrant.
 In normal times many democracies might find that too intrusive. Times are not normal.
 South Korea did well over a quarter of a million tests.
By the time South Korea had done 200,000 tests, 
we had probably done less than 1,000.

Disease spectrum

  • ~80% of infections are not severe and some may be asymptomatic.
  • Illnesses caused by the virus are primarily upper and lower respiratory tract infections.
  • For hospitalized patients with pneumonia, limited studies suggest the disease course (Wuhan experience):
    • ~50% develop hypoxemia by day 8
    • ARDS develops in 17-29%
    • Patients in the ICU require:
      • Non-invasive ventilation (42%)
      • Mechanical ventilation (47%)
      • High-flow O2 (11%)
      • ECMO (2-5%)
  • Critical Illness experience (Washington State)[7]
    • Small patient series (n = 21)
      • age: 70 (mean)
      • comorbidities: in 86%
      • Duration of symptoms: 3.5d (mean)
        • Admission to ICU within 24h of hospitalization: 81%
      • Nearly all had radiographic abnormalities at presentation
        • Leukopenia: in 67% ( decrease in disease-fighting cells in your blood)
      • Mechanical ventilation: in 71%
        • ARDS in 100% of those who required mechanical ventilation, most developed within 72h.
      • Most patients were not in shock, but 67% received Vasopressors 
      • Cardiomyopathy: developed in 33%
        • Unclear if direct viral effect v. critical illness stress
      • Mortality: 67% (as of publication date)
        SOURCE

Watching this relatively young guy, gasping for air, pink frothy secretions coming out of his tube and out of his mouth. The ventilator should have been doing the work of breathing but he was still gasping for air, moving his mouth, moving his body, struggling. We had to restrain him. With all the coronavirus patients, we’ve had to restrain them. They really hyperventilate, really struggle to breathe. When you’re in that mindstate of struggling to breathe and delirious with fever, you don’t know when someone is trying to help you, so you’ll try to rip the breathing tube out because you feel it is choking you, but you are drowning.

“When someone has an infection, I’m used to seeing the normal colors you’d associate with it: greens and yellows. The coronavirus patients with ARDS have been having a lot of secretions that are actually pink because they’re filled with blood cells that are leaking into their airways. They are essentially drowning in their own blood and fluids because their lungs are so full. So we’re constantly having to suction out the secretions every time we go into their rooms.”

....... you can’t adjust the ventilator settings as aggressively because you’re not going into the room as often. And we’re also trying to avoid going into the room as much as possible to reduce infection risk of staff and to conserve personal protective equipment.”

.......Your risk of mortality increases every day that you spend on a ventilator. The high pressures from high vent settings is pushing air into the lung and can overinflate those little balloons. They can pop. It can destroy the alveoli. Even if you survive ARDS, although some damage can heal, it can also do long-lasting damage to the lungs. They can get filled up with scar tissue. ARDS can lead to cognitive decline. Some people’s muscles waste away, and it takes them a long time to recover once they come off the ventilator.  SOURCE

=================

Severe pneumonia of any sort can cause shock and other organ damage. But in a webinar last week, Chinese doctors told members of the American College of Cardiology to watch for some additional problems in severe COVID-19, especially in people with heart disease. The worst off may need blood thinners as their blood starts to abnormally clot, and the heart itself may sustain damage not just from lack of oxygen but from the inflammation engulfing the body.

  Aug 4th Out of Control  Cykotine, B and T cells

May 28th May Be a Blood Vessel Disease -- the difference between SARS and SARS-CoV-2 likely stems from an extra protein each of the viruses requires to activate and spread.
Although both viruses dock onto cells through ACE2 receptors, another protein is needed to crack open the virus so its genetic material can get into the infected cell.
The additional protein the original SARS virus requires is only present in lung tissue, but the protein for SARS-CoV-2 to activate is present in all cells, especially endothelial cells.
In SARS1, the protein that’s required to cleave it is likely present only in the lung environment, so that’s where it can replicate. To my knowledge, it doesn’t really go systemic.
 SARS-CoV-2 is cleaved by a protein called furin, and that’s a big danger because furin is present in all our cells, it’s ubiquitous.”

May 1st Of the 8910 patients with Covid-19 for whom discharge status was available at the time of the analysis, a total of 515 died in the hospital (5.8%) and 8395 survived to discharge.

The factors we found to be independently associated with an increased risk of in-hospital death were

  • an age greater than 65 years (mortality of 10.0%, vs. 4.9% among those 65 years of age; odds ratio, 1.93; 95% confidence interval [CI], 1.60 to 2.41),
  • coronary artery disease (10.2%, vs. 5.2% among those without disease; odds ratio, 2.70; 95% CI, 2.08 to 3.51),
  • heart failure (15.3%, vs. 5.6% among those without heart failure; odds ratio, 2.48; 95% CI, 1.62 to 3.79),
  • cardiac arrhythmia (11.5%, vs. 5.6% among those without arrhythmia; odds ratio, 1.95; 95% CI, 1.33 to 2.86),
  • chronic obstructive pulmonary disease (14.2%, vs. 5.6% among those without disease; odds ratio, 2.96; 95% CI, 2.00 to 4.40), and
  • current smoking (9.4%, vs. 5.6% among former smokers or nonsmokers; odds ratio, 1.79; 95% CI, 1.29 to 2.47).

No increased risk of in-hospital death was found to be associated with the use of
ACE inhibitors
(2.1% vs. 6.1%; odds ratio, 0.33; 95% CI, 0.20 to 0.54)
or the use of
ARBs
(6.8% vs. 5.7%; odds ratio, 1.23; 95% CI, 0.87 to 1.74).

April 22 Wash. Post: A mysterious blood-clotting complication is killing COVID-19 patients

Apr 6th: Kaiser:- Mysterious Heart Damage, Not Just Lung Troubles, Befalling COVID-19 Patients
 Study found cardiac damage in as many as 1 in 5 patients, leading to heart failure and death even among those who show no signs of respiratory distress.
Infection can mimic a heart attack. They have taken patients to the cardiac catheterization lab to clear a suspected blockage, only to find the patient wasn’t really experiencing a heart attack but had COVID-19.

According to co-author Dr Zhibo Liu from Jinyintan Hospital, China:
"
Older age, showing signs of sepsis on admission, underlying diseases like high blood pressure and diabetes, and the prolonged use of non-invasive ventilation were important factors in the deaths of these patients.

Poorer outcomes in older people may be due, in part, to the age-related
weakening of the immune system and increased inflammation that could promote viral replication and more prolonged responses to inflammation, causing lasting damage to the heart, brain, and other organs.
Source The Lancet

Studies of COVID-19 patients found that 23 percent of those who were critically ill also suffered from cardiac "injury". The study did not conclude that the virus caused the cardiac injuries, however, just that they appeared together.

Rather than having a heart attack as suspected, some patients were actually found to have myocarditis, which results in similar changes to troponin levels and on an ECG.

Myocarditis is the inflammation of the heart muscle, and while it may be reassuring to find that a patient is not having a heart attack, myocarditis can still cause damage to the heart and result in irregular heart rhythms.

Sepsis is a potentially life-threatening condition caused by the body's response to an infection.
The body normally releases chemicals into the bloodstream to fight an infection.

Sepsis
 occurs when the body's response to these chemicals is out of balance,
triggering changes that can damage multiple organ systems

" the length of stay in cases who died in ICU in China -- 28 days on average"

First Symptom - Oxygen Level Falling ?

And here is what really surprised us: These patients did not report any sensation of breathing problems, even though their chest X-rays showed diffuse pneumonia and their oxygen was below normal. How could this be?

We are just beginning to recognize that Covid pneumonia initially causes a form of oxygen deprivation we call “silent hypoxia” — “silent” because of its insidious, hard-to-detect nature.

Pneumonia is an infection of the lungs in which the air sacs fill with fluid or pus. Normally, patients develop chest discomfort, pain with breathing and other breathing problems. But when Covid pneumonia first strikes, patients don’t feel short of breath, even as their oxygen levels fall. And by the time they do, they have alarmingly low oxygen levels and moderate-to-severe pneumonia (as seen on chest X-rays). Normal oxygen saturation for most persons at sea level is 94 percent to 100 percent; Covid pneumonia patients I saw had oxygen saturations as low as 50 percent.

To my amazement, most patients I saw said they had been sick for a week or so with fever, cough, upset stomach and fatigue, but they only became short of breath the day they came to the hospital. Their pneumonia had clearly been going on for days, but by the time they felt they had to go to the hospital, they were often already in critical condition.

In emergency departments we insert breathing tubes in critically ill patients for a variety of reasons. In my 30 years of practice, however, most patients requiring emergency intubation are in shock, have altered mental status or are grunting to breathe. Patients requiring intubation because of acute hypoxia are often unconscious or using every muscle they can to take a breath. They are in extreme duress. Covid pneumonia cases are very different.

A vast majority of Covid pneumonia patients I met had remarkably low oxygen saturations at triage — seemingly incompatible with life — but they were using their cellphones as we put them on monitors. Although breathing fast, they had relatively minimal apparent distress, despite dangerously low oxygen levels and terrible pneumonia on chest X-rays.

We are only just beginning to understand why this is so. The coronavirus attacks lung cells that make surfactant. This substance helps the air sacs in the lungs stay open between breaths and is critical to normal lung function. As the inflammation from Covid pneumonia starts, it causes the air sacs to collapse, and oxygen levels fall. Yet the lungs initially remain “compliant,” not yet stiff or heavy with fluid. This means patients can still expel carbon dioxide — and without a buildup of carbon dioxide, patients do not feel short of breath.

Patients compensate for the low oxygen in their blood by breathing faster and deeper — and this happens without their realizing it. This silent hypoxia, and the patient’s physiological response to it, causes even more inflammation and more air sacs to collapse, and the pneumonia worsens until oxygen levels plummet. In effect, patients are injuring their own lungs by breathing harder and harder.

Twenty percent of Covid pneumonia patients then go on to a second and deadlier phase of lung injury. Fluid builds up and the lungs become stiff, carbon dioxide rises, and patients develop acute respiratory failure.

By the time patients have noticeable trouble breathing and present to the hospital with dangerously low oxygen levels, many will ultimately require a ventilator.

Silent hypoxia progressing rapidly to respiratory failure explains cases of Covid-19 patients dying suddenly after not feeling short of breath. (It appears that most Covid-19 patients experience relatively mild symptoms and get over the illness in a week or two without treatment.)

A major reason this pandemic is straining our health system is the alarming severity of lung injury patients have when they arrive in emergency rooms. Covid-19 overwhelmingly kills through the lungs. And because so many patients are not going to the hospital until their pneumonia is already well advanced, many wind up on ventilators, causing shortages of the machines. And once on ventilators, many die.

A $40 MONITOR FOR YOUR OXYGEN LEVEL

The Accuracy of 6 Inexpensive Pulse Oximeters Not Cleared by the Food and Drug Administration: The Possible Global Public Health Implications

Detecting silent hypoxia early through a common medical device that can be purchased : a pulse oximeter.  display: oxygen saturation and pulse rate.

When they noticed their oxygen levels declining, both went to the hospital and recovered. Detection of hypoxia, early treatment and close monitoring apparently also worked for Boris Johnson. An early warning system.

SOURCE NYT April 20th

 An alternative hypothesis, developed by Dennis Shanks of the Australian Army Malaria Institute, in Queensland, and John Brundage of the Armed Forces Health Surveillance Centre, in Maryland.
This is that, in some circumstances, early exposure to a virus can harm subsequent immune responses rather than helping them.

Learning the wrong lesson

Dr Shanks and Dr Brundage observed that in 1890, the birth year of those who were 28 in 1918, a different and less lethal strain of influenza, known as Russian flu, spread around the world.

They also knew from experiments on pigs, conducted by others, that exposure to one virus during early life has the potential to make infections of other, quite different, viruses later on much more severe than they otherwise would have been.

Based on these observations they argued that the immune systems of those exposed to Russian flu as newborn babies—a period of life when immune systems are especially attuned to learning about which pathogens are circulating—learnt about Russian flu all too well.
As a consequence, when faced 28 years later with Spanish flu viruses they mounted the wrong response (ie, to Russian flu rather than to the real threat).

Nor is the example of 1918 unique. According to Dr Gagnon, people who were themselves born during that epidemic showed increased vulnerability to the Hong Kong flu of 1968.
And those born during the Asian flu of 1957 showed higher mortality in the face of swine flu in 2009.

He therefore wonders if something similar is going on now, with elderly people mounting inappropriate immune responses that reflect the infections of their youth.
Since all of his examples relate to influenza viruses, which are different beasts from coronaviruses, this is speculation.
But it is a line of inquiry that might be worth following once the immediate crisis is over.

SOURCE Economist

 

===========================================================================================================

As cases of coronavirus infection proliferate around the world and governments take extraordinary measures to limit the spread, there is still a lot of confusion about what exactly the virus does to people’s bodies.

The symptoms — fever, cough, shortness of breath — can signal any number of illnesses, from flu to strep to the common cold. Here is what medical experts and researchers have learned so far about the progression of the infection caused by this new coronavirus — and what they still don’t know.

How does this coronavirus cause infection?

The virus is spread through droplets transmitted into the air from coughing or sneezing, which people nearby can take in through their nose, mouth or eyes. The viral particles in these droplets travel quickly to the back of your nasal passages and to the mucous membranes in the back of your throat, attaching to a particular receptor in cells, beginning there.

Coronavirus particles have spiked proteins sticking out from their surfaces, and these spikes hook onto cell membranes, allowing the virus’ genetic material to enter the human cell.

That genetic material proceeds to “hijack the metabolism of the cell and say, in effect, ‘Don’t do your usual job. Your job now is to help me multiply and make the virus,’” said Dr. William Schaffner, an infectious disease specialist at Vanderbilt University Medical Center in Nashville, Tennessee.

How does that process cause respiratory problems?

As copies of the virus multiply, they burst out and infect neighboring cells. The symptoms often start in the back of the throat with a sore throat and a dry cough.

The virus then “crawls progressively down the bronchial tubes,” Schaffner said. When the virus reaches the lungs, their mucous membranes become inflamed. That can damage the alveoli or lung sacs, and they have to work harder to carry out their function of supplying oxygen to the blood that circulates throughout our body and removing carbon dioxide from the blood so that it can be exhaled.

“If you get swelling there, it makes it that much more difficult for oxygen to swim across the mucous membrane,” said Dr. Amy Compton-Phillips, the chief clinical officer for the Providence Health System, which included the hospital in Everett, Washington, that had the first reported case of the coronavirus in the United States, in January.

The swelling and the impaired flow of oxygen can cause those areas in the lungs to fill with fluid, pus and dead cells. Pneumonia, an infection in the lung, can occur.

Some people have so much trouble breathing, they need to be put on a ventilator. In the worst cases, known as Acute Respiratory Distress Syndrome, the lungs fill with so much fluid that no amount of breathing support can help, and the patient dies.

What trajectory does the virus take in the lungs?

Dr. Shu-Yuan Xiao, a professor of pathology at the University of Chicago School of Medicine, has examined pathology reports on coronavirus patients in China. He said the virus appears to start in peripheral areas on both sides of the lung and can take a while to reach the upper respiratory tract, the trachea and other central airways.

Xiao, who also serves as the director of the Center For Pathology and Molecular Diagnostics at Wuhan University, said that pattern helps explain why in Wuhan, where the outbreak began, many of the earliest cases were not identified immediately.

The initial testing regimen in many Chinese hospitals did not always detect infection in the peripheral lungs, so some people with symptoms were sent home without treatment.

“They’d either go to other hospitals to seek treatment or stay home and infect their family,” he said. “That’s one of the reasons there was such a wide spread.”

A recent study from a team led by researchers at the Icahn School of Medicine at Mount Sinai in New York found that more than half of 121 patients in China had normal CT scans early in their disease. That study and work by Xiao show that as the disease progresses, CT scans show “ground glass opacities,” a kind of hazy veil in parts of the lung that are evident in many types of viral respiratory infections. Those opaque areas can scatter and thicken in places as the illness worsens, creating what radiologists call a “crazy paving” pattern on the scan.

Are the lungs the only part of the body affected?

Not necessarily. Compton-Phillips said the infection can spread through the mucous membranes, from the nose down to the rectum.

So while the virus appears to zero in on the lungs, it may also be able to infect cells in the gastrointestinal system, experts say. This may be why some patients have symptoms like diarrhea or indigestion. The virus can also get into the bloodstream, Schaffner said.

The Centers for Disease Control and Prevention says that RNA from the new coronavirus has been detected in blood and stool specimens, but that it’s unclear whether infectious virus can persist in blood or stool.

Bone marrow and organs like the liver can become inflamed too, said Dr. George Diaz, section leader for infectious diseases at Providence Regional Medical Center in Everett, Washington, whose team treated the first U.S. coronavirus patient. There may also be some inflammation in small blood vessels, as happened with SARS, the viral outbreak in 2002 and 2003.

“The virus will actually land on organs like the heart, the kidney, the liver, and may cause some direct damage to those organs,” Schaffner said. As the body’s immune system shifts into high gear to battle the infection, the resulting inflammation may cause those organs to malfunction, he said.

As a result, some patients may endure damage that is inflicted not just by the virus but by their own immune system as it rages to combat the infection.

Experts have not yet documented whether the virus can affect the brain. But scientists who studied SARS have reported some evidence that the SARS virus could infiltrate the brain in some patients. Given the similarity between SARS and COVID-19, the infection caused by the new coronavirus, a paper published last month in the Journal of Medical Virology argued that the possibility that the new coronavirus might be able to infect some nerve cells should not be ruled out.

Why do some people get very ill but most don’t?

About 80% of people infected with the new coronavirus have relatively mild symptoms. But about 20% of people become more seriously ill; and in about 2% of patients in China, which has had the most cases, the disease has been fatal.

Experts say the effects appear to depend on how robust or weakened a person’s immune system is. Older people or those with underlying health issues, like diabetes or another chronic illness, are more likely to develop severe symptoms.

Xiao conducted pathological examinations of two people in China who went into a hospital in Wuhan in January for a different reason — they needed surgery for early-stage lung cancer — but whose records later showed that they had also had coronavirus infection, which the hospital did not recognize at the time. Neither patient’s lung cancer was advanced enough to kill them, he said.

One of those patients, an 84-year-old woman with diabetes, died from pneumonia caused by coronavirus, Xiao said the records showed.

The other patient, a 73-year-old man, was somewhat healthier, with a history of hypertension that he had managed well for 20 years. Xiao said the man had successful surgery to remove a lung tumor, was discharged, and nine days later returned to the hospital because he had a fever and cough that was determined to be the coronavirus.

Xiao said that the man had almost certainly been infected during his first stay in the hospital, since other patients in his post-surgical recovery room were later found to have the coronavirus. Like many other cases, it took the man days to show respiratory symptoms.

The man recovered after 20 days in the hospital’s infectious disease unit. Experts say that when patients like that recover, it is often because the supportive care — fluids, breathing support and other treatment — allows them to outlast the worst effects of the inflammation caused by the virus.

What do scientists still not know about coronavirus patients?

A lot. Although the illness resembles SARS in many respects and has elements in common with influenza and pneumonia, the course a patient’s coronavirus will take is not yet fully understood.

Some patients can remain stable for over a week and then suddenly develop pneumonia, Diaz said. Some patients seem to recover but then develop symptoms again.

Xiao said that some patients in China recovered but got sick again, apparently because they had damaged and vulnerable lung tissue that was subsequently attacked by bacteria in their body. Some of those patients ended up dying from a bacterial infection, not the virus. But that didn’t appear to cause the majority of deaths, he said.

Other cases have been tragic mysteries. Xiao said he personally knew a man and woman who got infected but seemed to be improving. Then the man deteriorated and was hospitalized.

“He was in ICU, getting oxygen, and he texted his wife that he was getting better, he had good appetite and so on,” Xiao said. “But then in the late afternoon, she stopped receiving texts from him. She didn’t know what was going on. And by 10 p.m., she got a notice from the hospital that he had passed.”

This article originally appeared in The New York Times.   Pam Belluck

==================================================================================

Most cases are mild, but the new virus is proving lethal to some

By Carolyn Y. Johnson Feb. 19, 2020 at 10:30 a.m. PST  Source: Source:- Washington Post

The mounting toll of coronavirus deaths, involving health-care workers on the front lines of the disease and older people in hospitals, raises a basic question: How does the new virus make people sick, and why does it kill some of them?

No one knows exactly how or why the novel coronavirus leads to death in just a small percentage of patients — about 2 percent of those infected, according to preliminary numbers. Based on what we know about related illnesses, including severe acute respiratory syndrome (SARS), experts hypothesize that the difference between a lethal infection and one that feels like a bad cold probably hinges on the interaction between the virus and a person’s immune system.

Killed by your own Immune system

While the virus attacks and kills cells in all cases, serious illness will depend on how the immune system responds, and that can be influenced by age, gender, genetics and underlying medical conditions. The initial damage caused by the virus can trigger a powerful and counterproductive overreaction by the immune system itself.

“What you get is the initial damage and rush of inflammatory cells, but the damage is so extensive that the body’s immune response is completely overwhelmed — which causes even more immune response, more immune cells and more damage,” said Matthew Frieman, a virologist at the University of Maryland School of Medicine.

The coronavirus is spread when an infected person sneezes or coughs, spraying droplets through the air. The sick person might sneeze directly in another person’s face or expel droplets widely, contaminating surfaces that healthy people touch before unknowingly spreading germs to their mouths or noses. Health-care workers are at especially high risk because they are exposed to very high doses of the virus and also perform procedures — such as putting patients on ventilators to help them breathe — that can spread it.

With infection, the virus probably begins to multiply inside cells lining the airway, which are fringed with hairlike structures. Coronaviruses that cause common colds are excellent at infecting the upper airway, while SARS tended to go deeper in the lungs. As the coronavirus gains strength, Frieman said, dead cells are sloughed off and collect in the airway, making breathing difficult.

“If the virus replicates very quickly, before your body has a chance to try and prevent it with an immune response, or if the immune response comes in too late, then it can’t control the virus and starts going berserk,” said Anthony Fehr, a virologist at the University of Kansas.

This is what scientists refer to as a “cytokine storm,” which causes the immune system to start sending cells ready to do battle into the lung. At that point, it’s not just the virus doing damage to the body; the immune system begins wreaking havoc on the infected person — also known as the “host” in medical parlance.

“The experience with other respiratory viruses would suggest it is a combination of the virus doing damage to the airways, secondary infections and the interplay with the host immune response,” said Erica S. Shenoy, an infectious diseases specialist at Massachusetts General Hospital.

The general risk factors for this mismatch between the immune system and any respiratory illness include advanced age and underlying chronic illnesses, including diabetes and high blood pressure, though public health experts are eager to understand more about who is most vulnerable in the current outbreak.

“Every individual is different,” Fehr said, and there are differences in how young and old or male and female immune systems react. “There are lots of dynamics at play when you talk about each individual and how they might die from this virus or why they might survive.”

Problems can also stack up. Vineet Menachery, a virologist at the University of Texas Medical Branch, suspects that the coronavirus may work much like SARS. When the virus gets deep into the lungs, it can damage alveoli, the air sacs that take in oxygen. As cellular damage accumulates, lung tissue begins to stiffen. The heart must work harder to get limited oxygen to the rest of the organs.

“What makes this new virus so damaging is you’re losing lung function, and that puts a strain on every organ in your body,” Menachery said.

Immunity?

In the patients who recover, the immune system’s response has worked: It has cleared the virus, with inflammation receding. Yet experts don’t know the long-term outcome for these individuals. It’s possible they will gain immunity and be protected from reinfection. Or they might get a less severe case in the future — or not be protected at all. They also might just gain temporary immunity. It’s yet another unanswered question about the coronavirus.

Missing from this article is the Immunity acquired by patients recovered from SARS !
...."Cumulative evidence suggests that patients who recovered from SARS possessed specific 
acquired immunity"....

• COVID Blood ClottingH1N1 Flu Pandemic 2009How COVID-19 KillsWe’re not going back to normalDrug Trials for COVIDOxygen instead of VentilatorSweden’s GDP reduced by 9.7% and Costa Rica’s by only 3.6% •    
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