Role of inflammatory markers in corona virus disease (COVID-19) patients: A review

Abstract

<jats:p> The whole world is locked down due to the outbreak of novel Coronavirus Disease 2019 (nCOVID-19). A novel virus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of coronavirus pandemic 2019. Investigating the role of inflammatory mediators and understanding the virology of nCOVID-19 virus help in designing a rational and effective therapy for this infection. This review provides an overview of the inflammatory mediators activated during nCOVID-19 infection and the pathophysiology of this viral infection. In this review, the authors have a detailed discussion about the types of viral strains of nCOVID-19, its mechanism of action, host immune response, and the dysregulation caused by the viruses in the host immune system causing disease progression. Understanding the role of inflammatory cytokines, chemokines, and clinical immunology will be the approach to find out the possible novel therapeutic interventions. Therapies involving regulation of immune responses help in inhibiting the various steps in the pathologies of infection. Also, updated knowledge regarding the dysregulation of immune system and disease outcome in critically ill patients serves as a precautionary measure in the development and evaluation of vaccine. </jats:p><jats:sec><jats:title>Impact statement</jats:title><jats:p> In late 2019, a novel virus called SARS-CoV-2, expanded globally from Wuhan, China and was declared a pandemic on 11 March 2020 by the WHO. The mechanism of virus entry inside the host cell depends upon the cellular proteases including cathepsins, HAT, and TMPRSS2, which splits up the spike protein and causes further penetration. MERS coronavirus uses DPP4, while coronavirus HCoV-NL63 and SARS-CoV and SARS-CoV-2 employ ACE-2 as the key receptor. Cytokine storm syndrome was analyzed in critically ill nCOVID-19 patients and it is presented with high inflammatory mediators, systemic inflammation, and multiple organ failure. Among various inflammatory mediators, the level of interleukins (IL-2, IL-7, IL-10), G-CSF, MIP1A, MCP1, and TNF-α was reported to be higher in critically ill patients. Understanding this molecular mechanism of ILs, T cells, and dendritic cells will be helpful to design immunotherapy and novel drugs for the treatment of nCOVID-19 infection. </jats:p></jats:sec>

Cytokine Storm and Mucus Hypersecretion in COVID-19: Review of Mechanisms

“… 18 Since mucin is quite large, it is packaged in secretory vesicles in a dehydrated state. 8 The release of mucin is governed by fusion proteins such as SNARE (N-ethyl-maleimide-sensitive factor attachment protein receptor) and MARCKS (Myristoylated Alanine-Rich C Kinase Substrate). The secretion occurs in the presence of high pH and low calcium concentration.…”

Advancement in biosensors for inflammatory biomarkers of SARS-CoV-2 during 2019–2020

“…In cytokine storm syndrome, the excessive release of cytokines or inflammatory biomarkers is observed ( Lingeswaran et al, 2020 ). The inflammatory biomarkers have been shown to be playing role in the COVID-19 infections also ( Upadhyay et al, 2020 ). Meta-analysis of the available data reveals the involvement of inflammatory biomarkers such as C-reaction protein (CRP), procalcitonin (PCT), interleukin-6 (IL-6) and ferritin (FT) ( Feng et al, 2020 ; Vaseghi et al, 2020 ; Zeng et al, 2020 ) in COVID-19 infections.…”

Treatment Modalities of the Covid-19 Pandemic Through Repurposed Drugs and Status of Vaccines

“…On the same day, the WHO declared Corona Virus Disease-19 (COVID- 19), the official name of the virus causing the disease [8,9]. The WHO declared a pandemic on March 11, 2020 [10]. COVID-19 is a modern disorder that has distinct biological features, clinical signs, and manifestations of the imaging, while important clinical management advancements have been achieved [11].…”