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“Cytokine storms” were a common feature of the 1918 flu, historians and health professionals say. But what is the role of potentially fatal immune responses in the coronavirus pandemic?
About 500 million people, or a third of the world’s population, were infected with the Spanish flu of 1918. An estimated 50 million people have died worldwide, with approximately 675,000 deaths occurring in the United States, according to the Centers for Disease. Control and Prevention. As of Saturday, 56.7 million people around the world have contracted COVID-19, with 1.3 million deaths, 244,987 of them in the United States.
These scientists aimed to find out. Most adults with moderate to severe COVID-19 have a suppressed viral immune response than those with the flu, according to research published Saturday by scientists at St. Jude Children’s Research Hospital in Memphis, Tennessee, and Washington University. School of Medicine in St. Louis, Mo.
Less than 5% of the COVID-19 patients in this study, including some of the sickest individuals, had the life-threatening hyperinflammatory immune response known as cytokine storm syndrome. Cytokines are small proteins secreted by blood cells that help coordinate the immune response and trigger inflammation, “he found.
“We identified a subset of COVID-19 patients with the largely upregulated range of cytokines, which is a hallmark of the cytokine storm,” said coauthor Paul Thomas, Ph.D., a member of the St. . “But, overall, the average person with COVID-19 – even patients with moderate to severe disease – had less inflammation than the average person with the flu.
He said patients would benefit from a quick, reliable, and inexpensive test to measure cytokines and identify those that are most likely to benefit from immunosuppressive treatment. “The results suggest that treatment that suppresses inflammation may only be effective in that minority of patients with the hyperinflammatory profile,” added Thomas.
Medical staff treat a coronavirus patient in the COVID-19 intensive care unit at United Memorial Medical Center on November 10, 2020 in Houston, Texas. COVID-19 infections are on the rise in Houston, Texas has passed 1 million cases.
Go to Nakamura / Getty Images
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A hallmark of some viruses: a surge of immune cells and their activating compounds (known as “cytokines”) actually turned the body against itself, led to inflammation of the lungs, severe respiratory distress, leaving the body vulnerable to secondary bacterial pneumonia. It was seen as one of the reasons apparently healthy people were so badly hit by the 1918 flu.
The research included 168 adults with COVID-19, 26 adults with influenza, and 16 healthy volunteers. More than 90% of COVID-19 patients were hospitalized, about half in the intensive care unit; 23% of the hospitalized died. More than half of influenza patients were hospitalized, 35% in intensive care and 8% of hospitalized influenza patients died.
The study found that the antiviral-immune response was “deeply suppressed” in COVID-19 patients compared with flu patients. In most cases, COVID-19 was not caused by extensive cytokine storm hyperinflammation, he said, but a lack of hyperinflammation in most of these coronavirus patients didn’t mean they had fewer diseases.
Doctors and members of the public, as of now, were frightened by how otherwise strong and healthy people fell victim to the 1918 flu, also known incorrectly as “Spanish flu”. Many historians today attribute this to the “cytokine storm,” the process in which the immune system in healthy people reacts so strongly that it damages the body.
“There are two hypotheses to explain the high lethality of the 1918 strain: cytokine storms and secondary bacterial infection,” according to a 2018 editorial in Nature. “In a cytokine storm, the body’s immune system overreacts, causing tissue and organ damage and even death.” However, the editorial says secondary bacterial infections are more likely to have played a bigger role.
The Nature editorial cites this “intriguing” 2008 paper published in the Journal of Infectious Diseases, which examined and reviewed over 8,400 tissue samples from 1918-1919 flu deaths found that “most of the deaths in the influenza pandemic of 1918-1919 is probably derived directly from secondary bacteria. Pneumonia caused by common upper respiratory tract bacteria. “
This could coincide with the progress of that pandemic with the second wave hitting even harder. “The second wave of the Spanish flu in 1918 was even more devastating than the first wave,” Ravina Kullar, an infectious disease expert at the Infectious Diseases Society of America and faculty member at the University of California, Los Angeles, told MarketWatch. .
Although the 1918 pandemic is forever associated with Spain, this strain of H1N1 flu was actually first discovered in Germany, France, the UK and the US, but similar to the Communist Party’s response to the first COVID-19 cases in Wuhan. in China, the last Decembert, World War I censorship buried or downplayed those earlier reports.
“It is essential to view the deep connections between the Great War and the influenza pandemic not simply as simultaneous or consecutive crises, but more deeply intertwined,” wrote historian James Harris around 1918. Members of the public were frightened by how otherwise strong, healthy people fell victim to the 1918 flu. A “cytokine storm” seemed like a likely explanation.
“There are two hypotheses to explain the high lethality of the 1918 strain: cytokine storms and secondary bacterial infection,” according to a 2018 editorial in Nature.
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The most recent study published Saturday, published in Science Advances, an open access peer-reviewed journal published by the American Association for the Advancement of Science, suggests that most COVID-19 patients are not candidates for steroid treatment such as dexamethasone, which researchers argue, can backfire in some patients.
Dexamethasone, however, has been shown to be effective in treating seriously ill COVID-19 patients, according to three studies published in September in JAMA. Researchers reported in mid-June that low-dose dexamethasone played a significant role in helping to reduce deaths in ventilator-hospitalized COVID-19 patients by a third.
Other research finds that cytokine storms remain a risk for older patients during the 2020 coronavirus pandemic. According to research published in August in the Journal of Molecular and Cellular Cardiology, genes in the body that appear to be a major contributing factor SARS-CoV-2 access to heart cells become more active with age, according to research published in August in the Journal of Molecular and Cellular Cardiology.
The researchers found that “inflammation in older people can be more intense, causing organ damage,” Johns Hopkins University reported. “Lung tissue becomes less elastic over time, making respiratory diseases such as COVID-19 a particular concern for older people.” Therefore, a cytokine storm in those patients can promote inflammation and acute respiratory distress syndrome.
Additionally, a September 2020 article published in the peer-reviewed journal Frontiers in Immunology concluded: “Aberrant immune host response along with cytokine storm and lymphocytopenia, [a disorder where your blood does not have enough white blood cells] followed by acute respiratory distress, are still relevant issues affecting the severity of COVID-19. “
A similar one exists between 1918 and 2020: During the 1918 flu, cities that implemented non-pharmaceutical interventions such as social distancing and school closures tended to have better economic outcomes, wrote Francis Yared, global research manager. on rates at Deutsche Bank in a recent note, adding: “There was not such a big trade-off between economic activity and public health.”
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