Year-end Sale % OFF 
Abstract
In December 2019, the first case of patient with severe acute respiratory syndrome (SARS) caused by the novel coronavirus, SARS-CoV-2, was reported in Wuhan, Hubei Province, Central China. SARS-CoV-2 causes CoronaVirus Disease-2019 (COVID-19 or nCoV-19) disease, which rapidly spread all over the world. In response to this serious situation, on 30 January 2020, the World Health Organization (WHO) declared a global public health emergency of international concern, putting all health organizations on high alert. In mid-March 2020, WHO declared nCoV-19 a pandemic. By the end of September 2020, there were ~33.67 million confirmed cases and ~10.08 lakh deaths worldwide and the trend rising on each passing day. SARS-CoV-2 mainly infects the pulmonary system, but cause damage to other organs such as heart, kidney and intestine. Understanding the cardio-pulmonary issues underpinning of nCOV-19 pathogenesis is key to managing outcomes and mortality. SARS-CoV-2 uses the SARS-CoV receptor ACE2 for entry and the serine protease inhibitor TMPRSS2 for S protein priming. Alveolar cells and cardiomyocytes express ACE2 and TMPRSS2. In this Review, we summarize the current understanding of nCOV-19 pandemic from basic mechanisms to clinical perspectives, focusing on the interaction between SARS-CoV-2 and the cardio-pulmonary-immune signatures. The study provides crucial insights into the first step of SARS-CoV-2 infection, and potential targets for antiviral intervention.
Highlights
History of severe acute respiratory syndrome (SARS)-CoV-2Coronaviruses (CoVs) have been identified as human pathogens since early 1960
Alveolar cells and cardiomyocytes express angiotensin-converting enzyme-2 (ACE2) and TMPRSS2. In this Review, we summarize the current understanding of nCOV-19 pandemic from basic mechanisms to clinical perspectives, focusing on the interaction between SARS-CoV-2 and the cardio-pulmonary-immune signatures
In some of the most severe SARS-CoV-2 infected patients, the cytokine storm, combined with a diminished capacity to pump oxygen to the rest of the body, can result in pulmonary edema, acute cardiac, renal or hepatic injury and death [32]. These studies were supported by a recent study from Ziegler group [24], wherein the authors reported that ACE2 receptors are induced by interferon-γ, thereby amplifying the infectious cycle in the lungs
Summary
Coronaviruses (CoVs) have been identified as human pathogens since early 1960. CoVs belong to the subfamily Orthocoronavirinae in the family Coronaviridae, order Nidovirales. Considering the global threat, on January 30, 2020 the WHO has declared nCoV-19 pandemic a public health emergency of international concern (PHEIC) It has been nine months since health officials reported spread of mysterious invisible SARS-CoV-2 infection in China. Genome structure of SARS-CoV-2 The SARS-CoV-2 is an enveloped, positive-sense, single-stranded RNA genome named for its solar corona like appearance [13]. Besides TMPRSS2, endosomal protease cathepsin-L (CTS-L) enhances SARS-CoV-2 entry into host alveolar cells and cardiomyocytes [20]. This observation was supported by the fact that, cathepsin B/L involved in vascular remodeling and cardiovascular diseases [21]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
