COVID-19 Cytokine Storm is Different From Other Respiratory Infections
Hyper-induction of pro-inflammatory cytokines is one of the key aspects of SARS-CoV-2.
When we become infected with a virus like COVID-19, our immune system often goes into overdrive and can lead to a life-threatening cycle known as a cytokine storm. The SARS-CoV-2 virus, like other respiratory infections, catalyzes this overactive immune response for its own benefit.
Recently, investigators from Earlham Institute (EI) and the Quadram Institute, in collaboration with Korcsmaros Group, have discovered significantly important differences between the COVID-19 cytokine storm and the cytokine storms of other respiratory viral infections. The results from their study were published in the journal Frontiers in Immunology.
"As the onset of the cytokine storm is one of the key factors behind the mortality rates we're seeing in a particular group of COVID-19 patients, it is critical to understand why it is happening" Marton Olbei, a project leader at the Korcsmáros Group said. "Cytokine storms are not unique to SARS-CoV-2 infection; they can be found in most of the critical human coronaviruses and influenza. A subtype outbreaks of the past two decades."
The investigators behind the study analyzed over 5,000 studies to find which ones contained data on immune responses from patients so that they could find key differences in different cytokine storms. The team looked for changes in cytokine patterns in those who had been infected with various respiratory infections, including COVID-19.
Findings showed that the SARS-CoV-2 virus had a unique tendency to stop the rise of specific cytokines in certain patients when compared to other similar viruses. Although it has distinct similarities to influenza and other types of coronaviruses, COVID-19 targets specific regulators of the cytokine response that can lead to more severe disease. The investigators discovered that this was not due to the virus itself, but the specific immune response in certain patients.
"For a subgroup of patients, when infected by these viruses, a real danger is posed by the immune system overreacting,” Olbei said. “We're drawing out which specific parts of our immune system react in a potentially harmful way to these viruses.”
The discovery of these immune responses could potentially aid clinical specialists in identifying interventions that could help to alleviate the cytokine storm and evaluate how effective they could be.
"We wanted to take a step back and summarize what is actually being reported in the scientific literature, specifically focusing on cytokine-mediated immune responses, to put into context and differentiate SARS-CoV-2 from these other viruses,” Olbei said. “Building up a data repository such as this will also be vital for the future; if other similar viruses arose, you could quickly find their profile and compare."