However, the level gradually increases mainly because the patients encounter clinical deterioration with respiratory failure along with an increase in additional biomarkers (e.g., interleukin-6, ferritin, and lactate dehydrogenase) IL2RG and usually occurs during the second week of hospitalization. neurologic disease [1]. Six coronavirus varieties were previously known to cause human being disease [1]. Four viruses-229E, OC43, NL63, and HKU1-typically cause mild respiratory illness in immunocompetent individuals; whereas, the additional two betacoronaviruses-severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV)-have been linked to fatal illnesses in the past two decades [1,2]. SARS-CoV was the causal agent of the severe acute respiratory syndrome outbreaks in 2002 and 2003 in Guangdong province, China. MERS-CoV was the pathogen responsible for severe respiratory disease outbreaks in 2012 in the Middle East and has been responsible for more than 10,000 cumulative instances in the past two decades; mortality rates of 10% for SARS-CoV and 37% for MERS-CoV have been reported [1-3]. In December 2019, the first pneumonia instances of unknown source were recognized in Wuhan, the capital city of Hubei province, China. These instances were epidemiologically linked to a local Huanan wholesale seafood market [1,2]. A previously unfamiliar betacoronavirus was found out through unbiased sequencing MK-0557 in samples from individuals with pneumonia. Human being airway epithelial cells were used to isolate a novel enveloped RNA betacoronavirus, named 2019-nCoV, and later on renamed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) created a clade within the subgenus sarbecovirus, orthocoronavirinae subfamily [1]. Phylogenetic analysis showed that SARS-CoV-2 offers 89% genome sequence identity to a bat SARS-like coronavirus, 80% identity to SARS and 50% identity to MERS coronavirus, therefore making SARS-CoV-2 the seventh member of the coronavirus family that infects humans, as well as the third coronavirus with bat origins [4]. Since its initial identification, the disease caused by SARS-CoV-2, coronavirus disease 2019 (COVID-19) offers spread to more than 187 countries worldwide over the past few months [5]. Given the rapid spread of this computer virus, with effects on an international scale, COVID-19 was declared a pandemic from the World Health Business on March 11, 2020 [6]. As of May 10, 2020, more than four million COVID-19 instances were reported globally (including more than 1.3 million cases in the United States), which are associated with more than 281,000 deaths to day [5]. Although SARS-CoV-2 appears to have a lower fatality rate than either SARS-CoV or MERS-CoV, COVID-19 has resulted in many more deaths than both of these prior outbreaks combined, partly because of its higher infectivity (estimated reproductive quantity (R0) of between 2 and 3) and higher assault rate, therefore leading to more infected individuals [6]. Evidence of person to person transmission has been observed, primarily through close contact and respiratory droplets. The virus can be detected one to two days before sign onset in top respiratory samples, and the median incubation period has been estimated to be 5.1 days (95% confidence interval (CI), 4.5-5.8 days) [7]. Although most symptomatic individuals with COVID-19 present with fever, dry cough and shortness of breath, and display pneumonia on imaging findings, approximately of ten percent of patients possess a worsening of the disease, thus requiring rigorous care and possible complications such as acute respiratory stress syndrome (ARDS), viremia, acute cardiac injury, disseminated intravascular coagulation (DIC), multi-organ failure and subsequent death in critically ill individuals [8]. Definition of acute myocardial injury Myocardial injury is definitely defined as an elevation in cardiac biomarkers, cardiac troponin I (TnI) or troponin T (TnT) above the 99th percentile of the top research limit, and is considered acute if there is a rise and/or fall in cardiac troponin concentrations exceeding the biological and/or analytical variance; myocardial injury may be secondary to ischemic or nonischemic processes [9,10]. Traditionally, elevated troponin concentrations have been considered equivalent to myocardial infarction. However, with improvements in troponin assays, elevated levels without overt symptoms or indicators MK-0557 of myocardial ischemia are now more common; hence, the fourth universal definition of myocardial infarction considers myocardial injury to be a independent, unique MK-0557 entity [11]. Based on current evidence,.