Why do some people get so sick with COVID-19, while others have benign symptoms? Three key molecules appear to play a key role, new research revealed this week.
All of these important indicators, all found in the blood of critically ill patients, may be characterized as specific cytokines, or hormone-like molecules produced by cells. immunity in the body can modulate the immune response. When overproduced, cytokines accelerate inflammation and can cause serious results.
Their scientific names won’t make much sense to the average reader – EN-RAGE, TNFSF14 and oncostatin-M – but researchers at Stanford University School of Medicine, in collaboration with others in Atlanta and Hong Kong, believes these specific molecules can help illuminate exactly what happens in the body̵7;s immune system when it fights COVID-19.
“One of the great mysteries of COVID-19 infection is that some people develop severe illness,” said Bali Pulendran, senior author of the study and professor of pathology, microbiology and immunology at Stanford. while others seem to be recovering quickly. “We now have some insight into why that happened.”
Researchers have found higher levels of those molecules in the blood of critically ill patients. Scientists are currently working to suppress the action of these molecules as potential therapies for the disease, hoping to help critically ill patients with their immune systems overreacting to microbes. withdraw.
The study, published in Science on Tuesday, looked at the immune system responses of 76 COVID-19 and 69 uninfected patients from Princess Margaret Hospital at the University of Hong Kong and the Clinic. Hope at Emory University in Atlanta.
When an infection such as COVID-19 is present, the body’s innate immune system produces cytokines, which help the body fight off viruses. When too much cytokine is produced, it causes the immune system to malfunction and begin to attack the body, and that can produce life-threatening symptoms.
Three specific molecules found in high concentrations in patients with the most severe illness were previously unidentified in those with COVID-19, Stanford research found. Researchers are currently testing therapeutic drugs that target these molecules as a potential treatment. A drug that inhibits the activity of the TNFSF14 molecule, also known as LIGHT, is believed to reduce inflammation. It is similar to the anti-inflammatory steroid dexamethasone, praised for improving outcomes for patients with extremely severe, but more targeted, and possibly more effective coronaviruses against one of the produced molecules. of these patients is the greatest.
Pulendran and other Stanford researchers are doing a study testing the drug in hamsters in September. If successful, they’ll test it on non-human primates, then humans. .
Research has also shown that there is a lot of bacterial debris in the blood of patients with extremely severe COVID-19 disease. These study authors believe these go from the lungs or intestines to the bloodstream, suggesting the far-reaching effects of the infection. Scientists suspect the debris contributes to the overproduction of molecules found in critically ill patients. They hope another study on the progression of the disease will reveal more.
Another surprising discovery was found by the study’s authors: Despite widespread inflammation in the lungs of extremely sick patients, their blood innate immune systems were suppressed. . Researchers want to study what this means for already recovered COVID-19 patients, such as whether they might be susceptible to blood-borne infections.
Although researchers now know more about what happens in the body’s immune system when someone becomes seriously ill with COVID-19, it’s unclear what caused that response. People with health conditions, such as diabetes, are more likely to get worse results, but how those risk factors affect the state of a person’s immune system have not been studied yet. study carefully, Pulendran said. The study did not have a large enough sample to evaluate the impact, he added.
Pulendran and colleagues, in collaboration with Emory researchers, are now recruiting hundreds of frontline health workers without COVID-19 in a baseline study to collect blood samples every two weeks. If any of the participants became infected, researchers would study whether anything different in those patients’ immune systems could make them more likely to develop the disease.
This study helps shed light on the sometimes bewildering experiences of tens of thousands of people in the Gulf that have been infected with the virus. That includes a Sunnyvale family, who both have COVID-19, with a wide range of symptoms.
Connie Lares Ruspini, a medical interpreter at Lucile Packard Stanford Children’s Hospital, spent her birthday on April 7 checking her family’s temperature and oxygen levels and listening to their lungs. Her 16-year-old daughter Natalia felt tired, her body ached and had difficulty breathing. Her husband, Diego has a cough, fever and vomiting. Ruspini himself suffered from joint pain, mild fever and anorexia. Both husband and wife have diarrhea. Her son, Santiago, 12, had no symptoms – except to eat three times normal.
The family nanny, who had pre-existing conditions, including obesity, high blood pressure and diabetes, had dropped dangerously low oxygen levels and required special care for about 10 days. Diego, who has asthma, also spent a week breathing oxygen in the hospital.
Family tested negative in the first week of May. The nanny was given oxygen at home for six weeks after hospitalization and continued to have difficulty breathing, Ruspini said. Sometimes Diego still feels tired and tight in the chest. In contrast, Ruspini, making a full recovery, hiked up Mount Whitney on August 3.
“It was a terrible fear in this family,” said Ruspini. “I hope people take this seriously… because it can be very devastating. We are lucky, even though we have a household and get sick, but everyone makes it through ”.
Mallory Moench is a chronicle writer of the San Francisco Chronicle. Email: firstname.lastname@example.org Twitter: @mallorymoench