According to the latest research by Yale University, the differing immune system responses of patients with COVID-19 can help predict who is going to experience moderate and severe consequences of the disease. The findings may be resourceful and help identify individuals at high risk of severe illness earlier in their hospitalization and suggest drugs to treat COVID-19.
The researchers examined 113 patients admitted to Yale New Haven Hospital. They analyzed the patients’ differing immune system responses during their hospital stay, from the time of admittance to discharge until death.
The team found that all the patients shared a common COVID-19 “signature symptom” in their immune system activity early in the course. But those who experienced only moderate symptoms showing diminishing immune system responses and viral load over time. Patients who went on to develop severe cases of the disease exhibited no reduction in viral load or immune system reaction. Many of the immune system signals in these patients accelerated.
But even in the first course of treatment, the team found indicators that predicted which patients were at the highest risk of developing severe forms of illness. Akiko Iwasaki, the Waldemar Von Zedtwitz Professor of Immunobiology and Molecular and Development Biology Investigator for the Howard Hughes Medical Institute, claimed that the team was able to pull out signatures of the disease risk.
The researchers had known that the immune system unleashes a vast and damaging “cytokine storm” in severe cases of COVID-19. But these elements of the immune system response most responsible for the damage were unknown. The analysis found some interesting links to poor outcomes. Curiously, one risk factor was the presence of alpha interferon; a cytokine mobilized to combat viral pathogens like the flu virus. However, COVID-19 patients with high levels of alpha interferon fared worse than those with low levels.
Researchers explained that the virus doesn’t seem to care about alpha interferon. The cytokine appears to be hurting, not helping. Another prognosticator of poor outcomes is the activation of the inflammasome, a complex of proteins that detects pathogens and triggers an inflammatory response to infection. Inflammasome activation was linked to poor results and even death in several patients.
The team also found that people who respond better to the infection tend to express high levels of growth factors, a type of cytokine that repairs tissue damage to the linings of blood vessels and lungs. Together, the data can help predict patients at high risk of poor outcomes. They also said drugs that target specific causes of inflammation identified in the study could help treat the patients at risk of developing severe cases of COVID-19.