Comparison of SARS-CoV-2 and influenza cytokine storm

In a recent study published in Interferon & Cytokine Research JournalResearchers compared the cytokine storms of pandemic influenza and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.

study: Comparison of COVID-19 and Pandemic Influenza Cytokine Storm.. Image credit: NIAID

Background

The new respiratory virus poses a serious health risk as it can cause large-scale outbreaks. The SARS-CoV-2 pandemic has resulted in millions of severe infections and deaths worldwide over the last two years. Both vaccination against 2019 coronavirus disease (COVID-19) and spontaneous infection have been shown to provide a protective immune response against SARS-CoV-2, but the parameters affecting prevalence are well understood. Not.

Matching the immune fingerprints of SARS-CoV-2 infections with the immune fingerprints of other severe respiratory infections such as pandemic influenza resolves the current debate as to why those severe symptoms are behind. May be useful for. As a result, finding similarities in the immunopathology of the two diseases may lead to immunotherapeutic targets that address common pathogenic processes. On the other hand, identifying the distinctive characteristics that distinguish each infection can lead to the discovery of specific immune modifications that support the diagnosis of each instance and the development of personalized therapies.

About research

In the current study, researchers consider cytokine storms as the root cause of pathological conditions and summarize the immunopathological components of pandemic influenza and COVID-19. The team analyzed the differences and similarities in the cytokine signatures of both infectious diseases and identified compounds that were more attractive to the development of translated and pharmaceutical products.

This review will look up Cytokine storm The syndrome (CSS) between influenza and COVID-19 identifies a conserved immunopathogenic process that underpins severe illness. In addition, researchers relate to specific cytokine systems involved in the etiology of COVID-19 by highlighting distinct immune properties in severe SARS-CoV-2 infections and presenting potential immunotherapeutic targets. Shows the theoretical basis for future research.

The mechanism behind the cytokine storm of sepsis. Sepsis is an exaggerated immune response triggered by a local or systemic infection. People in this state show elevated levels of cytokines in the circulation (hypercytokine storms). This is a phenomenon called “cytokine storm”. Mechanisms are under investigation to facilitate the progression of sepsis from the normal immune response to pathogens. The clinical and demographic characteristics of affected individuals may contribute to the pathological biology of sepsis, along with genetic factors that promote excessive immune activation or influence the regulatory mechanisms of the immune system. there is. Extensive production of cytokines results in adverse effects on local cells, activation, and increased endothelial permeability, as well as microthrombosis. Hypercytokine storms are also associated with many anti-inflammatory mechanisms that disrupt immune cell function (immune paralysis). Together, these changes (cytokine storm + immune paralysis) lead to the development of organ failure without eliminating the infection. Understanding the etiology of sepsis is important for addressing other severe infections such as COVID-19 and pandemic influenza. The artwork used in this figure is Biorender (https://biorender.com/), Licensed under the Creative Commons Attribution 3.0 Unported License. COVID-19, Coronavirus disease 2019.

Results and conclusions

Overall, the data reported in this article show significant differences and similarities in the immune signatures of severe COVID-19 and influenza. In addition, both diseases increase the levels of cytokines that have different roles.

Elevated cytokines such as interferon β (IFN-β) and IFN-α have antiviral properties, and tumor necrosis factor α (TNFα), interleukin 22 (IL-22), IL-12) are severe SARS. Shows inflammatory properties-CoV-2 and influenza infection. In addition, IL-10 has regulatory functions, and fibroblast growth factor (FGF) and platelet-derived growth factor (PDGF) have angiogenic properties. In addition, cytokines such as chemokine (CXC motif) ligand 8 (CXCL8), CXCL10, CXCL9, chemokine (CC motif) ligand 2 (CCL2), CCL5, and CCL4 have chemotactic properties. In addition, granulocyte colony stimulating factor (G-CSF), PDGF, and FGF are characteristic of growth factors.

Therefore, the authors suggest that pathogenic processes such as increased innate immune stimulation, microvascular dysfunction, monocyte or neutrophil chemotaxis may be associated with COVID-19 and influenza disease. I paid attention to. Using the information presented in this review, we can conclude that the CSS for severe COVID-19 and influenza are similar, suggesting an equivalent pathogenic pathway that can be used for therapeutic purposes.

Indeed, both viruses are recognized by the same pattern recognition receptor (PRR), activate similar signaling pathways, and require equivalent adaptive and innate immune components for protection. Elevated inflammasomes such as IL-1, TNF, IL-6 and PRR-induced cytokines are found in severe COVID-19 and influenza CS, suggesting a chronic congenital inflammatory cascade that is detrimental to the host. .. If these compounds are addressed, they can reduce the immunological and vascular effects important in the pathophysiology of sepsis, alleviate inflammation, and allow extrapulmonary organs and lungs to reestablish equilibrium. There is sex.

Cytokine storm profile of pandemic influenza and COVID-19. (A) Cytokines, chemokines, and growth factors that are commonly or differentially elevated between severe influenza and COVID-19 have been identified by retrospective analysis of independent studies. (B) An immune profile that distinguishes COVID-19 from influenza identified by parallel comparison. The artwork used in this figure is Biorender (https://biorender.com/), Licensed under the Creative Commons Attribution 3.0 Unported License.

Conversely, there was a disparity between COVID-19 and influenza immune fingerprints. Type 1 T-helper (Th1) cytokines and IL-2, growth-inducing ligand (APRIL), soluble tumor necrosis factor receptor 2 (sTNF-R2), sTNF-R1, CXCL17, and surfactant protein D (SP-D) severe influenza patient. In addition, patients with severe SARS-CoV-2 exhibit a multifunctional Th2 / Th1 / Th17 immune activation pattern. According to the findings, SARS-CoV-2, not the influenza virus, induced a multifunctional and abundant CS profile.

As a result, restoring a balanced immune response may be a viable goal of host-oriented therapy for a partial subset of SARS-CoV-2 patients. The team found that the optimal COVID-19 immunotherapeutic agent restores useful immune homeostasis that blocks specific immune signaling pathways associated with hyperinflammation and enhances protective immunity in a subset of patients that produce multifunctional cytokines. Suggest that you need to.

The authors further identify these immune characteristics and further determine the ideal time to provide a particular immunotherapy based on the cytokine kinetics of these diseases (SARS-CoV-2 and influenza infections). He said research is needed. They need to evaluate in future studies whether tesepermab, which improves lung function and reduces exacerbation and eosinophilia in people with uncontrolled asthma, can improve the outcome of COVID-19. Said.