Fatal ReincaRNAtion of VIRUS causing COronaVIrus disease.

Abstract

Coronaviridae-family viruses are enveloped positive-strand RNA viruses and were previously known to cause mild respiratory illness in humans and other mammals until the year 2002, when a fatal outbreak of severe acute respiratory syndrome (SARS)CoV emerged via wild cats in China. The outbreak infected many people and caused more than 750 deaths. This outbreak was also responsible for tremendous economic losses around the world. Ten years after this incident, in the year 2012 in Saudi Arabia another coronavirus emerged known as Middle East respiratory syndrome (MERS) which caused more than 800 deaths. Then, in the year 2019, another coronavirus known as SARS-CoV-2 emerged in China and caused a worldwide pandemic which affected almost all of the countries in the world leading to millions of deaths around the globe. This special issue of International Reviews of Immunology focuses on various aspects of SARS-CoV-2 and host interaction in terms of the development of immune responses such as various degrees of inflammation, antibody responses, and effects on host physiology. This issue also discusses approaches to diagnosis through quali t at ive and quant i t at ive es t imat ion of SARS-CoV-2-associated immune molecular signatures. Additionally, a few articles in this issue also discuss different aspects of SARS-CoV-2 vaccine development (Figure 1). Coronavirus disease 19 (COVID) has a wide range of symptoms ranging from mild to severe. Mild symptoms include runny nose, fever or chills, cough, sore throat, congestion, fatigue, headache, taste or smell loss, body aches, nausea or vomiting, and sometimes diarrhea, shortness of breath or difficulty in breathing. The severe symptoms include trouble in breathing, discomfort, pain or pressure in the chest area, inability to wake or stay awake, and pale, gray, or blue-coloured skin and lips. Notably, many infected individuals remain asymptomatic, while in contrast, a small percentage of the population die due to COVID. Considering this wide variation in disease outcomes, it is interesting to understand the complex interplay among the various components of host immunity to SARS-CoV-2. The article by Negia et al discusses the immune responses that develop toward variants of the SARS-CoV-2 infection. Upon infection the virus induces both innate and adaptive immune responses to control infection. However, overwhelmed immune responses lead to severe complications. The article also notes that SARS-CoV-2 infection also induces B and T cell responses to induce strong antibody responses. The article by Mallano et al discusses how antibody responses can be exploited for the diagnosis and treatment of COVID. The article also discusses how this knowledge can be helpful in vaccine development. The SARS-CoV-2 infection primarily induces various levels of inflammation which skews host physiology and vitals. The skewed host physiology can dysregulate immune cells or immune responses or, vice versa, cause various complications including cytokine storm or coagulopathy. The article by Landau et al discusses various immune signaling pathways that can induce inflammation and their direct or indirect involvement in coagulopathy. The article provides an insight into how a dysregulated immune system impacts host physiology and can culminate in immunopathologic responses. SARS-CoV-2 infection in individuals with various preexisting diseases such as other infectious diseases, noninfectious diseases like cancer, autoimmune diseases, and metabolic diseases cause different impacts on host physiology and subsequently overall disease outcome in terms of disease severity. The article by Naqvi et al