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Respiratory viruses like SARS-CoV-2 (which causes COVID-19) can often catalyze an overactive immune response that leads to a life-threatening cycle, known as a cytokine storm.
Analysis of the cytokine responses of patients infected with SARS-CoV-2 and similar common respiratory viruses has uncovered remarkably important differences in how SARS-CoV-2 affects cytokines compared to other common respiratory viruses.
The comprehensive data resource is intended to help specialists identify better treatments and diagnoses of the underlying causes that can cause the deadly cytokine storm.
Scientists from the Earlham Institute (EI) and the Quadram Institute are studying how the immune system responds to infection with SARS-CoV-2 and other similar respiratory viruses, in particular to identify unique characteristics in severely ill COVID-19 patients.
Members of the Korcsmaros Group working alongside clinical virologist Claire Shannon-Lowe at the University of Birmingham focused their attention on how SARS-CoV-2 and other respiratory viruses are causing the so-called ‘cytokine storm’, a hyperactivation of our Own immune system – one of the main reasons for the high death rate in a subset of COVID-19 patients.
To identify the similarities and differences in the cytokine storm, the researchers collected and analyzed the vast collection of thousands of COVID-19 research papers. They looked for patterns of cytokine changes in patients who had been infected by respiratory viruses that cause cytokine release syndrome.
By systematically analyzing more than 5,000 scientific studies to find those that contain patient immune response data, the researchers demonstrated that SARS-CoV-2 has a unique tendency to stop the rise of specific cytokines in certain patients compared to other viruses. Similar. This is important in understanding the causes of the potentially fatal cytokine release syndrome, more commonly known as a cytokine storm.
“Given that the onset of the cytokine storm is one of the key factors behind the mortality rates that we are seeing in a particular group of COVID-19 patients, it is critical to understand why it is happening,” said the doctoral student. project leader Marton Olbei. in the Korcsmáros Group.
“Cytokine storms are not unique to SARS-CoV-2 infection; they can be found in most critical human coronaviruses and influenza. A subtype of outbreaks from the past two decades.”
Cytokines are small proteins that tightly regulate our immune system and how our body reacts to internal or external stress, such as cancer, inflammation, or infection. Cytokines act as drivers, orchestrating our immune response when infected with viruses. One of its functions is to cause inflammation, which is part of the healing process for many infections and injuries.
All respiratory viruses activate antiviral responses in the body, but there are differences in the way each virus tries to evade the immune system’s attention. The most common strategy is to confuse or specifically target crucial immune response mechanisms, such as cytokine release.
A cytokine storm occurs only in the immune system of certain patients when they react to a virus. A feedback loop causes continuous activation of the cytokines responsible for inflammation, resulting in organ failure or even death.
While SARS-CoV-2 cases have distinct similarities to both influenza patients and those who were infected in previous coronavirus outbreaks (SARS-CoV, MERS-CoV), the researchers’ analysis found specific immune mechanisms that make SARS-CoV-2 especially dangerous.
We examined the changing levels of cytokines following infection with similar viral pathogens (SARS-CoV, MERS-CoV, H5N1, H7N9) to highlight the unique and protective cytokine responses caused by these viruses. “
Marton Olbei, PhD student and project manager, Grupo Korcsmáros
By comparing the immune response data of COVID-19 patients, the researchers found cumulative similarities against these pathogens, which discriminate between influenza A and coronavirus subtypes, and the unusual aspects of the currently circulating SARS-CoV-2 virus. .
SARS-CoV-2 is similar to other respiratory viruses but, by targeting specific regulators of the cytokine response, with only small-scale differences, it could lead to more severe disease, not from the virus itself, but from the response of the patient’s immune system. .
“For a subset of patients, when they are infected by these viruses, the immune system overreacts as a real danger. We are determining which specific parts of our immune system react in a potentially harmful way to these viruses,” Marton said.
“We wanted to take a step back and summarize what is actually reported in the scientific literature, focusing specifically on cytokine-mediated immune responses, to contextualize and differentiate SARS-CoV-2 from these other viruses. Creating a data repository like this will also be vital for the future, if other similar viruses emerged, I could quickly find their profile and compare. “
A map of such immune responses could help clinicians identify interventions that have successfully alleviated cytokine storms in other diseases and assess whether they could be effective in treating certain cases of COVID-19.
Source:
Magazine reference:
Olbei, M., et al. (2021) SARS-CoV-2 causes a different cytokine response compared to other respiratory viruses that cause cytokine storms in seriously ill patients. Frontiers in immunology. doi.org/10.3389/fimmu.2021.629193.
