scholarly journals Comparison of Selected Characteristics of SARS-CoV-2, SARS-CoV, and HCoV-NL63

2021 ◽  
Vol 11 (4) ◽  
pp. 1497
Author(s):  
Darina Bačenková ◽  
Marianna Trebuňová ◽  
Tatiana Špakovská ◽  
Marek Schnitzer ◽  
Lucia Bednarčíková ◽  
...  

The global pandemic known as coronavirus disease 2019 (COVID-19) was caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This review article presents the taxonomy of SARS-CoV-2 coronaviruses, which have been classified as the seventh known human pathogenic coronavirus. The etiology of COVID-19 is also briefly discussed. Selected characteristics of SARS-CoV-2, SARS-CoV, and HCoV-NL63 are compared in the article. The angiotensin converting enzyme-2 (ACE-2) has been identified as the receptor for the SARS-CoV-2 viral entry. ACE2 is well-known as a counter-regulator of the renin-angiotensin system (RAAS) and plays a key role in the cardiovascular system. In the therapy of patients with COVID-19, there has been a concern about the use of RAAS inhibitors. As a result, it is hypothesized that ACE inhibitors do not directly affect ACE2 activity in clinical use. Coronaviruses are zoonotic RNA viruses. Identification of the primary causative agent of the SARS-CoV-2 is essential. Sequencing showed that the genome of the Bat CoVRaTG13 virus found in bats matches the genome of up to (96.2%) of SARS-CoV-2 virus. Sufficient knowledge of the molecular and biological mechanisms along with reliable information related to SARS-CoV-2 gives hope for a quick solution to epidemiological questions and therapeutic processes.

Author(s):  
Jieqiong Wang ◽  
Huiying Zhao ◽  
Youzhong An

Angiotensin converting enzyme 2 (ACE2), a transmembrane glycoprotein, is an important part of the renin-angiotensin system (RAS). In the COVID-19 epidemic, it was found to be the receptor of severe acute respiratory syndrome coronavirus 2 (SARS-COV-2). ACE2 maintains homeostasis by inhibiting the Ang II-AT1R axis and activating the Ang I (1-7)-MasR axis, protecting against lung, heart and kidney injury. In addition, ACE2 helps transport amino acids across the membrane. ACE2 sheds from the membrane, producing soluble ACE2 (sACE2). Previous studies have pointed out that sACE2 plays a role in the pathology of the disease, but the underlying mechanism is not yet clear. Recent studies have confirmed that sACE2 can also act as the receptor of SARS-COV-2, mediating viral entry into the cell and then spreading to the infective area. Elevated concentrations of sACE2 are more related to disease. Recombinant human ACE2, an exogenous soluble ACE2, can be used to supplement endogenous ACE2. It may represent a potent COVID-19 treatment in the future. However, the specific administration concentration needs to be further investigated.


Author(s):  
Congqing Wu ◽  
Dien Ye ◽  
Adam E. Mullick ◽  
Zhenyu Li ◽  
A.H. Jan Danser ◽  
...  

AbstractAngiotensin-converting enzyme 2 (ACE2), a component of the renin-angiotensin system, is a receptor for SARS-CoV-2, the virus that causes COVID-19. To determine whether the renin-angiotensin inhibition regulates ACE2 expression, either enalapril (an angiotensin-converting enzyme inhibitor) or losartan (an AT1 receptor blocker) was infused subcutaneously to male C57BL/6J mice for two weeks. Neither enalapril nor losartan changed abundance of ACE2 mRNA in lung, ileum, kidney, and heart. Viral entry also depends on transmembrane protease serine 2 (TMPRSS2) to prime the S protein. TMPRSS2 mRNA was abundant in lungs and ileum, modest in kidney, but barely detectable in heart. TMPRSS2 mRNA abundance was not altered by either enalapril or losartan in any of the 4 tissues. Next, we determined whether depletion of angiotensinogen (AGT), the unique substrate of the renin-angiotensin system, changes ACE2 and TMPRSS2 mRNA abundance. AGT antisense oligonucleotides (ASO) were injected subcutaneously to male C57BL/6J mice for 3 weeks. Abundance of ACE2 mRNA was unchanged in any of the 4 tissues, but TMPRSS2 mRNA was significantly decreased in lungs. Our data support that the renin-angiotensin inhibition does not regulate ACE2 and hence are not likely to increase risk for COVID-19.


Author(s):  
Elham Foroozanfar ◽  
Mohamad Forouzanfar ◽  
Tahereh Farkhondeh ◽  
Saeed Samarghandian ◽  
Fatemeh Forouzanfar

Abstract:: A novel coronavirus termed nCoV-2019 caused an epidemic of acute respiratory syndrome in humans was first detected in Wuhan, China, in December 2019. nCoV-2019 resulted in thousands of cases of lethal disease all around the world. Unfortunately, there is no specific treatment yet so better understanding of the pathobiology of the disease can be helpful. The renin–angiotensin system and their products has several important physiological actions, On the other hand, this system involved in the pathogenesis of various diseases. In this context, this review article will briefly insights for understanding the role of angiotensin-converting enzyme 2 (ACE2) receptor as a potential attractive target for nCoV-2019- induced acute respiratory syndrome.


TH Open ◽  
2020 ◽  
Vol 04 (02) ◽  
pp. e138-e144 ◽  
Author(s):  
Wolfgang Miesbach

AbstractThe activated renin–angiotensin system induces a prothrombotic state resulting from the imbalance between coagulation and fibrinolysis. Angiotensin II is the central effector molecule of the activated renin–angiotensin system and is degraded by the angiotensin-converting enzyme 2 to angiotensin (1–7). The novel coronavirus infection (classified as COVID-19) is caused by the new coronavirus SARS-CoV-2 and is characterized by an exaggerated inflammatory response that can lead to severe manifestations such as acute respiratory distress syndrome, sepsis, and death in a proportion of patients, mostly elderly patients with preexisting comorbidities. SARS-CoV-2 uses the angiotensin-converting enzyme 2 receptor to enter the target cells, resulting in activation of the renin–angiotensin system. After downregulating the angiotensin-converting enzyme 2, the vasoconstrictor angiotensin II is increasingly produced and its counterregulating molecules angiotensin (1–7) reduced. Angiotensin II increases thrombin formation and impairs fibrinolysis. Elevated levels were strongly associated with viral load and lung injury in patients with severe COVID-19. Therefore, the complex clinical picture of patients with severe complications of COVID-19 is triggered by the various effects of highly expressed angiotensin II on vasculopathy, coagulopathy, and inflammation. Future treatment options should focus on blocking the thrombogenic and inflammatory properties of angiotensin II in COVID-19 patients.


2020 ◽  
Vol 126 (10) ◽  
pp. 1456-1474 ◽  
Author(s):  
Mahmoud Gheblawi ◽  
Kaiming Wang ◽  
Anissa Viveiros ◽  
Quynh Nguyen ◽  
Jiu-Chang Zhong ◽  
...  

Author(s):  
Annalise E Zemlin ◽  
Owen J Wiese

Since the first cases of atypical pneumonia linked to the Huanan Seafood Wholesale Market in Wuhan, China, were described in late December 2019, the global landscape has changed radically. In March 2020, the World Health Organization declared COVID-19 a global pandemic, and at the time of writing this review, just over three million individuals have been infected with more than 200,000 deaths globally. Numerous countries are in ‘lockdown’, social distancing is the new norm, even the most advanced healthcare systems are under pressure, and a global economic recession seems inevitable. A novel coronavirus (SARS-CoV-2) was identified as the aetiological agent. From experience with previous coronavirus epidemics, namely the severe acute respiratory syndrome (SARS) and Middle East Respiratory Syndrome (MERS) in 2004 and 2012 respectively, it was postulated that the angiotensin-converting enzyme-2 (ACE2) receptor is a possible port of cell entry. ACE2 is part of the renin-angiotensin system and is also associated with lung and cardiovascular disorders and inflammation. Recent studies have confirmed that ACE2 is the port of entry for SARS-CoV-2. Male sex, advanced age and a number of associated comorbidities have been identified as risk factors for infection with COVID-19. Many high-risk COVID-19 patients with comorbidities are on ACE inhibitors and angiotensin receptor blockers, and this has sparked debate about whether to continue these treatment regimes. Attention has also shifted to ACE2 being a target for future therapies or vaccines against COVID-19. In this review, we discuss COVID-19 and its complex relationship with ACE2.


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