Immune Profiling of COVID-19 in Correlation with SARS and MERS

Abstract

Acute respiratory distress syndrome (ARDS) is a major complication of the respiratory illness coronavirus disease 2019, with a death rate reaching up to 40%. The main underlying cause of ARDS is a cytokine storm that results in a dysregulated immune response. This review discusses the role of cytokines and chemokines in SARS-CoV-2 and its predecessors SARS-CoV and MERS-CoV, with particular emphasis on the elevated levels of inflammatory mediators that are shown to be correlated with disease severity. For this purpose, we reviewed and analyzed clinical studies, research articles, and reviews published on PubMed, EMBASE, and Web of Science. This review illustrates the role of the innate and adaptive immune responses in SARS, MERS, and COVID-19 and identifies the general cytokine and chemokine profile in each of the three infections, focusing on the most prominent inflammatory mediators primarily responsible for the COVID-19 pathogenesis. The current treatment protocols or medications in clinical trials were reviewed while focusing on those targeting cytokines and chemokines. Altogether, the identified cytokines and chemokines profiles in SARS-CoV, MERS-CoV, and SARS-CoV-2 provide important information to better understand SARS-CoV-2 pathogenesis and highlight the importance of using prominent inflammatory mediators as markers for disease diagnosis and management. Our findings recommend that the use of immunosuppression cocktails provided to patients should be closely monitored and continuously assessed to maintain the desirable effects of cytokines and chemokines needed to fight the SARS, MERS, and COVID-19. The current gap in evidence is the lack of large clinical trials to determine the optimal and effective dosage and timing for a therapeutic regimen.

A Gradient pH‐Sensitive Polymer‐Based Antiviral Strategy via Viroporin‐Induced Membrane Acidification

“…Recently, increasing studies indicate that the “cytokine storm” as an excessively activated inflammatory response contributes to the mortality of coronavirus disease 2019. [ 22 ] To explore the effects of the GPS 6.8 in alleviating inflammatory damage of host caused by coronavirus infection, we developed mouse models infected with mouse hepatitis viruses A59 (MHV‐A59), a β‐coronavirus that can mimic the infection of severe acute respiratory syndrome coronavirus (SARS‐CoV), Middle East respiratory syndrome coronavirus (MERS‐CoV) and SARS‐CoV‐2. [ 23 ] Similar to SARS‐CoV‐2, RNA‐seq analysis of differentially expressed genes in livers showed that the genes induced by MHV infection were enriched in inflammation pathways like leukocyte migration and anti‐bacterial pathways (Figure S6c, Supporting Information).…”

COVID-19 and the Immune Response: A Multi-Phasic Approach to the Treatment of COVID-19

“…The phenomenon of the cytokine storm, or hypercytokinemia, is not unique to COVID-19 infections, although it is a commonly cited cause of COVID-related mortality [ 87 , 88 ]. In essence, hypercytokinemia is characterized by three markers [ 89 ]: Perpetuated activation of lymphocytes and macrophages causing immune dysregulation; Large secretions of cytokines caused by such perpetuated activation; Overwhelming systemic inflammation and multi-organ failure with high mortality.…”

Cellular and Humoral Immunity and Infection Responses to SARS-CoV-2:Immune Biomolecular Mechanisms by Case Study within SARS-CoV-2 Pathogenesis and Other Infections

“…But also, transforming, and vascular endothelial cellular growth factors (TGF-β/VEGF)) along-side specific matrix metalloproteinases (MMP2, MMP3, MMP9) that represent tissue re-modelling proteins with specific chemotactic factors required to direct leukocyte chemotaxis between GC and throughout the body that include CXCL10 (IP-10), CCL2 (MCP-1), CCL3 (MIP1-α, and CCL11 [51][52][53][54][55]. However, in Middle East Respiratory Syndrome (MERS) IL-1β, IL-8, and IL-6 were highlighted whereas in SARS-CoV-2 CXCL10 does appear to be a key pleiotropic chemokine that has since been clarified in SARS-CoV-2 utilizing CXCR3 expressed on Mϕ, T cells, dendritic cells and both NK and B cells [56][57][58].…”