scholarly journals Supplementation with vitamin D in the COVID-19 pandemic?

2020 ◽  
Author(s):  
Fatemeh Hadizadeh
Keyword(s):  
Vitamin D ◽  
Angiotensin Converting Enzyme ◽  
Respiratory Infections ◽  
Renin Angiotensin System ◽  
Protective Role ◽  
Epidemiologic Studies ◽  
World Health ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Health Organization

Abstract The coronavirus disease 2019 (COVID-19) pandemic was declared a public health emergency of international concern by the World Health Organization. COVID-19 has high transmissibility and could result in acute lung injury in a fraction of patients. By counterbalancing the activity of the renin-angiotensin system, angiotensin-converting enzyme 2, which is the fusion receptor of the virus, plays a protective role against the development of complications of this viral infection. Vitamin D can induce the expression of angiotensin-converting enzyme 2 and regulate the immune system through different mechanisms. Epidemiologic studies of the relationship between vitamin D and various respiratory infections were reviewed and, here, the postulated mechanisms and clinical data supporting the protective role of vitamin D against COVID-19–mediated complications are discussed.

scholarly journals The Significance of Angiotensin-Converting Enzyme-2 (ACE2) in SARSCov-2 Infection and COVID-19

Coronaviruses ◽  
2020 ◽  
Vol 01 ◽  
Author(s):  
Carolina Restini ◽  
Trevor Belavek ◽  
Rafael Bernal ◽  
Vanessa Ibrahim ◽  
Kelly Irwin ◽  
...  
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Angiotensin Converting Enzyme ◽  
Renin Angiotensin System ◽  
Cell Receptor ◽  
Host Cells ◽  
World Health ◽  
Protective Effects ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Health Organization

: The new coronavirus was first reported in 2019 (China) and officially announced by the World Health Organization as a pandemic in March 2020. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the pneumonia-associated illnesses and shares structural homology with the related Severe acute respiratory syndrome coronavirus-1 (SARS-CoV-1). One of the mechanisms for SARS-Cov-1 and -2 infection is mediated by the angiotensin-converting enzyme-2 (ACE2) cell receptor, enabling the virus to enter the host cells. ACE2 is an isoform of the angiotensin-converting enzyme 1 (ACE). The actions of ACE2 counterbalance the classic renin-angiotensin system (RAS) axis through the production of Ang 1-7, which promotes cardiovascular, renal, and lung-protective effects. The ACE2 is not the only route for SARS-CoV-2 to enter the host cells. However, due to its roles in the RAS and its participation in the SARS-CoV-2 virulence, ACE2 has gained attention regarding viral mechanisms of pathogenesis, effects of drugs that interfere with the RAS, and as a potential target for therapeutic strategies for the damages caused by SARSCoV-2 infection. Among other tissues, ACE2 gene expression seems to be increased in the lungs upon SARS-CoV-2 infection; however, amid other variables, expression and/or activity of ACE2 is shown as a disease, sex, and age-dependent. The present review covers critical aspects for a comprehensive understanding of ACE2 and its current involvement in SARS-CoV-2 infection and the development of COVID-19.

scholarly journals Coronavirus disease 2019 (COVID-19) and the renin-angiotensin system: A closer look at angiotensin-converting enzyme 2 (ACE2)

2020 ◽  
Vol 57 (5) ◽  
pp. 339-350 ◽  
Author(s):  
Annalise E Zemlin ◽  
Owen J Wiese
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Angiotensin Receptor Blockers ◽  
Renin Angiotensin System ◽  
World Health ◽  
Atypical Pneumonia ◽  
Converting Enzyme ◽  
Wholesale Market ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin

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.

scholarly journals The mechanistic overview of SARS-CoV-2 using angiotensin-converting enzyme 2 to enter the cell for replication: possible treatment options related to the renin–angiotensin system

2020 ◽  
Vol 6 (5) ◽  
pp. 317-325 ◽  
Author(s):  
Annette Offringa ◽  
Roy Montijn ◽  
Sandeep Singh ◽  
Martin Paul ◽  
Yigal M Pinto ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Scientific Discovery ◽  
Treatment Options ◽  
Renin Angiotensin System ◽  
Practical Experience ◽  
Protective Role ◽  
Converting Enzyme ◽  
Negative Consequences ◽  
Theoretical Understanding ◽  
Angiotensin Converting Enzyme 2

Abstract The SARS-CoV-2 pandemic is a healthcare crisis caused by insufficient knowledge applicable to effectively combat the virus. Therefore, different scientific discovery strategies need to be connected, to generate a rational treatment which can be made available as rapidly as possible. This relies on a solid theoretical understanding of the mechanisms of SARS-CoV-2 infection and host responses, which is coupled to the practical experience of clinicians that are treating patients. Because SARS-CoV-2 enters the cell by binding to angiotensin-converting enzyme 2 (ACE2), targeting ACE2 to prevent such binding seems an obvious strategy to combat infection. However, ACE2 performs its functions outside the cell and was found to enter the cell only by angiotensin II type 1 receptor (AT1R)-induced endocytosis, after which ACE2 is destroyed. This means that preventing uptake of ACE2 into the cell by blocking AT1R would be a more logical approach to limit entry of SARS-CoV-2 into the cell. Since ACE2 plays an important protective role in maintaining key biological processes, treatments should not disrupt the functional capacity of ACE2, to counterbalance the negative effects of the infection. Based on known mechanisms and knowledge of the characteristics of SARS-CoV we propose the hypothesis that the immune system facilitates SARS-CoV-2 replication which disrupts immune regulatory mechanisms. The proposed mechanism by which SARS-CoV-2 causes disease immediately suggests a possible treatment, since the AT1R is a key player in this whole process. AT1R antagonists appear to be the ideal candidate for the treatment of SARS-CoV-2 infection. AT1R antagonists counterbalance the negative consequences of angiotesnin II and, in addition, they might even be involved in preventing the cellular uptake of the virus without interfering with ACE2 function. AT1R antagonists are widely available, cheap, and safe. Therefore, we propose to consider using AT1R antagonists in the treatment of SARS-CoV-2.

scholarly journals A plausible path to contain the spread of 2019 Novel Coronavirus; a computational analysis prompts to the use of ACE2 receptor blockers

2020 ◽  
Author(s):  
Christopher Whitman
Keyword(s):  
Angiotensin Converting Enzyme ◽  
World Health ◽  
Converting Enzyme ◽  
Time Sharing ◽  
Angiotensin Converting Enzyme 2 ◽  
Bioinformatic Tools ◽  
Receptor Blockers ◽  
Genetic Sequences ◽  
Novel Coronavirus ◽  
Health Organization

Abstract Starting December 30th, 2019, a virus spread from Wuhan, in the Hubei Province of China. The virus had soon been recognized as part of the Coronavirus and temporarily named 2019 Novel Coronavirus. The dramatic increase of infections led to the death of over 400 people, by Feb 4th, 2020. By this day the virus had already crossed into 27 countries. March 11th, 2020 the World Health Organization declared the Novel Coronavirus a pandemic, pointing to over 118,000 cases of infections in over 110 countries. This public health threat drove the international community to real-time sharing of the genetic sequences isolated from the viruses. We used these freely accessible genetic data, while leveraging bioinformatic tools, with the intent to explore possible contributions to address this threat. Angiotensin-converting Enzyme 2 Inhibition has been proven to be a valuable strategy address the spread of SARS. After proving remarkable genetic similarities between SARS and the 2019 Novel Coronavirus, we computationally built the first known ex-novo model of the 2019 Novel Coronavirus Spike Glycoprotein entirely generated from its aminoacidic sequence, using I-TASEER. We then assessed the 2019 Novel Coronavirus interaction with the human Angiotensin-converting Enzyme 2. This research prompts at the potential use of Angiotensin- converting Enzyme 2 receptors blockers, as both clinical and prophylaxis measures to contain the spread of 2019 Novel Coronavirus.

scholarly journals Identification of gene expression location of angiotensin‐converting enzyme‐2 SNPs as a receptor for SARS‐CoV‐2 in different populations by using various databases

2021 ◽  
Vol 26 (2) ◽  
pp. 101
Author(s):  
Dyah Aryani Perwitasari ◽  
Rita Maliza ◽  
Bayu Tri Murti ◽  
Haafizah Dania ◽  
Athika Darumas Putri
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Binding Capacity ◽  
Treatment Options ◽  
World Health ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Damage Level ◽  
Gene Variation ◽  
Health Organization ◽  
European Populations

The World Health Organization (WHO) has announced that Severe Acute Respiratory Syndrome Coronavirus‐2 (SARS‐CoV‐2) and Coronavirus disease (COVID‐19) is considered a worldwide pandemic. Rapidly rising numbers of patients have been reported in almost every country, along with the growing mortality rates. Uncontrolled growth in patient numbers may be due to reasons such as treatment options and vaccine availabilities and unidentified targets of SARS‐CoV‐2. Previous study has revealed that the molecular target of SARS‐CoV‐2 is analogous to SARS (2003), i.e. angiotensin‐converting enzyme‐2 (ACE‐2). Therefore, the determination of ACE‐2 may enrich existing information and facilitate development of drugs targeted toward SARS‐CoV‐2. This study aims to screen the expression of ACE‐2 genes and their relationship to the types of SNP variants in SARS‐CoV‐2. We explored a series of observations using powerful databases, e.g. GTEx portal, HaploReg, 1000 Genome and Ensembl, to identify the gene variant of ACE‐2. We showed that ACE‐2 is highly expressed in the testes and small intestine, while its lowest level is observed in lymphocytes. Subsequently, we observed 17 gene variants containing a missense mutation potentially damaging protein level. Among these genes, single nucleotide polymorphism (SNP) rs370187012 shows the highest damage‐level score, while the lowest effect is in SNP rs4646116. The highest frequency of the C allele was observed in European populations (1%). In addition to showing that ACE‐2 is expressed in several organs, we concluded that the ACE‐2 gene variation can be found in African, American, Southeast and East Asian, and European populations. The polymorphisms of ACE‐2 impact on the ACE2 protein structure and the binding capacity of the ACE‐2 receptor with the S‐Protein of SARS‐CoV‐2.

scholarly journals Angiotensin-Converting Enzyme 2 and COVID-19: Patients, Comorbidities, and Therapies

2020 ◽  
Author(s):  
Girish Pathangey ◽  
Priyal Praful Fadadu ◽  
Alexandra Raye Hospodar ◽  
Amr Abbas
Keyword(s):  
Risk Factors ◽  
Angiotensin Converting Enzyme ◽  
World Health ◽  
Converting Enzyme ◽  
Angiotensin Ii Receptor ◽  
Limited Evidence ◽  
Angiotensin Converting Enzyme 2 ◽  
Moderate Evidence ◽  
Receptor Blockers ◽  
Health Organization

On March 11, 2020, the World Health Organization declared COVID-19 a pandemic, and the reality of the situation has finally caught up to the widespread reach of the disease. The presentation of the disease is highly variable, ranging from asymptomatic carriers to critical COVID-19. The availability of angiotensin-converting enzyme 2 (ACE2) receptors may reportedly increase the susceptibility and/or disease progression of COVID-19. Comorbidities and risk factors have also been noted to increase COVID-19 susceptibility. In this paper, we hereby review the evidence pertaining to ACE2's relationship to common comorbidities, risk factors, and therapies associated with severe and critical COVID-19. We also highlight gaps of knowledge that require further investigation. The primary comorbidities of respiratory disease, cardiovascular disease, renal disease, diabetes, obesity, and hypertension had strong evidence. The secondary risk factors of age, sex, and genetics had limited-to-moderate evidence. The tertiary factors of ACE inhibitors and angiotensin II receptor blockers had limited-to-moderate evidence. Ibuprofen and thiazolidinediones had limited evidence.

scholarly journals Pathological Role of Angiotensin II in Severe COVID-19

TH Open ◽  
2020 ◽  
Vol 04 (02) ◽  
pp. e138-e144 ◽  
Author(s):  
Wolfgang Miesbach
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Treatment Options ◽  
Renin Angiotensin System ◽  
Target Cells ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
Novel Coronavirus

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.

scholarly journals Dysregulation of ACE (Angiotensin-Converting Enzyme)-2 and Renin-Angiotensin Peptides in SARS-CoV-2 Mediated Mortality and End-Organ Injuries

Hypertension ◽  
2021 ◽  
Author(s):  
Kaiming Wang ◽  
Mahmoud Gheblawi ◽  
Anish Nikhanj ◽  
Matt Munan ◽  
Erika MacIntyre ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Tumor Necrosis Factor Receptor ◽  
Renin Angiotensin System ◽  
Adverse Outcomes ◽  
Blood Collection ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
Angiotensin Peptides

ACE (angiotensin-converting enzyme)-2 as the target for SARS-CoV-2 also negatively regulates the renin-angiotensin system. Pathological activation of ADAM17 (A disintegrin and metalloproteinase-17) may potentiate inflammation and diminish ACE2-mediated tissue protection through proteolytic shedding, contributing to SARS-CoV-2 pathogenesis. We aim to examine plasma soluble ACE2 and angiotensin profiles in relation to outcomes by enrolling consecutive patients admitted for COVID-19 with baseline blood collection at admission and repeated sampling at 7 days. The primary outcome was 90-day mortality, and secondary outcomes were the incidence of end-organ injuries. Overall, 242 patients were included, the median age was 63 (52–74) years, 155 (64.0%) were men, and 57 (23.6%) patients reached the primary end point. Baseline soluble ACE2 was elevated in COVID-19 but was not associated with disease severity or mortality. In contrast, an upward trajectory of soluble ACE2 at repeat sampling was independently associated with an elevated risk of mortality and incidence of acute myocardial injury and circulatory shock. Similarly, an increase in soluble tumor necrosis factor receptor levels was also associated with adverse outcomes. Plasma Ang I, Ang 1-7 (angiotensin 1–7) levels, and the Ang 1-7/Ang II (angiotensin II) ratio were elevated during SARS-CoV-2 infection related to downregulation of ACE activity at baseline. Moreover, patients having an upward trajectory of soluble ACE2 were characterized by an imbalance in the Ang 1-7/Ang II ratio. The observed dysregulation of ACE2 and angiotensin peptides with disease progression suggest a potential role of ADAM17 inhibition and enhancing the beneficial Ang 1-7/Mas axis to improve outcomes against SARS-CoV-2 infection.

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