Gastrointestinal Tract and COVID-19

2022 ◽  
pp. 127-140
Author(s):  
Aaron Lelo Pambu ◽  
Abdellah Zinedine
Keyword(s):  
Virus Entry ◽  
Healthcare Systems ◽  
The Novel ◽  
Highly Pathogenic ◽  
Angiotensin Converting Enzyme 2 ◽  
Gastrointestinal Manifestations ◽  
Republic Of China ◽  
Current Outbreak ◽  
Novel Coronavirus

The current outbreak of the novel coronavirus, SARS-CoV-2 (coronavirus disease 2019; previously 2019- nCoV), epi-centered in Hubei Province of the People's Republic of China, has spread to many other countries caused an extreme burden for healthcare systems globally. Coronaviruses are traditionally considered nonlethal pathogens to humans, mainly causing approximately 15% of common colds. In this century, we have encountered highly pathogenic human CoVs twice. In this chapter, the authors propose to focus the gastrointestinal physiopathology of the infection of SARS-Cov2. This chapter will develop subject like the gastrointestinal manifestations of the infection to SARS-Cov2. The second part of this chapter will develop the role of the gut microbiome in the SARS-Cov2 diseases susceptibilities. And then the authors will show the etiopathogenesis of SARS-Cov2 associated diarrhea. As reported by previous studies, the SARS-Cov virus entry into host cell is mediated by the interaction between the envelop-anchored viral spike protein and the host receptor named angiotensin-converting enzyme 2 (ACE2).

scholarly journals Investigation of the genetic variation in ACE2 on the structural recognition by the novel coronavirus (SARS-CoV-2)

2020 ◽  
Author(s):  
Xingyi Guo ◽  
Zhishan Chen ◽  
Yumin Xia ◽  
Weiqiang Lin ◽  
Hongzhi Li
Keyword(s):  
Genetic Variation ◽  
The Novel ◽  
S Protein ◽  
Angiotensin Converting Enzyme 2 ◽  
Missense Variants ◽  
Catalytic Metal ◽  
Using Data ◽  
Novel Coronavirus ◽  
Insight Into

Abstract Background: The outbreak of coronavirus disease (COVID-19) was caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), through its surface spike glycoprotein (S-protein) recognition on the receptor Angiotensin-converting enzyme 2 (ACE2) in humans. However, it remains unclear how genetic variations in ACE2 may affect its function and structure, and consequently alter the recognition by SARS-CoV-2. Methods: We have systemically characterized missense variants in the gene ACE2 using data from the Genome Aggregation Database (gnomAD; N = 141,456). To investigate the putative deleterious role of missense variants, six existing functional prediction tools were applied to evaluate their impact. We further analyzed the structural flexibility of ACE2 and its protein-protein interface with the S-protein of SARS-CoV-2 using our developed Legion Interfaces Analysis (LiAn) program.Results: Here, we characterized a total of 12 ACE2 putative deleterious missense variants. Of those 12 variants, we further showed that p.His378Arg could directly weaken the binding of catalytic metal atom to decrease ACE2 activity and p.Ser19Pro could distort the most important helix to the S-protein. Another seven missense variants may affect secondary structures (i.e. p.Gly211Arg; p.Asp206Gly; p.Arg219Cys; p.Arg219His, p.Lys341Arg, p.Ile468Val, and p.Ser547Cys), whereas p.Ile468Val with AF = 0.01 is only present in Asian.Conclusions: We provide strong evidence of putative deleterious missense variants in ACE2 that are present in specific populations, which could disrupt the function and structure of ACE2. These findings provide novel insight into the genetic variation in ACE2 which may affect the SARS-CoV-2 recognition and infection, and COVID-19 susceptibility and treatment.

scholarly journals Arterial Hypertension as a Risk Comorbidity Associated with COVID-19 Pathology

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Alexander Kamyshnyi ◽  
Inna Krynytska ◽  
Victoriya Matskevych ◽  
Mariya Marushchak ◽  
Oleh Lushchak
Keyword(s):  
Arterial Hypertension ◽  
Pressure Control ◽  
The Novel ◽  
Global Public Health ◽  
Angiotensin Converting Enzyme 2 ◽  
Cardiovascular Comorbidities ◽  
Public Health Challenge ◽  
Novel Coronavirus ◽  
Ace2 Gene

Coronavirus disease 2019 (COVID-19), caused by the novel coronavirus severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), is an ongoing global public health challenge. Current clinical data suggest that, in COVID-19 patients, arterial hypertension (AH) is one of the most common cardiovascular comorbidities; it can worsen outcomes and increase the risk of admission to intensive care unit (ICU). The exact mechanisms through which AH contributes to the poor prognosis in COVID-19 are not yet clear. The putative relationship between AH and COVID-19 may be linked to the role of angiotensin-converting enzyme 2 (ACE2), a key element of the AH pathophysiology. Another mechanism connecting AH and COVID-19 is the dysregulation of the immune system resulting in a cytokine storm, mediated by an imbalanced response of T helper cells subtypes. Therefore, it is essential to optimize blood pressure control in hypertensive patients and monitor them carefully for cardiovascular and other complications for the duration of COVID-19 infection. The question whether AH-linked ACE2 gene polymorphisms increase the risk and/or worsen the course of SARS-CoV-2 infection should also receive further consideration.

COVID 19: Camostat and The Role of Serine Protease Entry Inhibitor TMPRSS2

2020 ◽  
Author(s):  
Stefan Bittmann
Keyword(s):  
Host Cell ◽  
Serine Protease ◽  
Cellular Protein ◽  
Host Cells ◽  
The Novel ◽  
Robert Koch Institute ◽  
Angiotensin Converting Enzyme 2 ◽  
Novel Coronavirus ◽  
Transmembrane Serine Protease

According to the latest research, the novel coronavirus uses the protein angiotensin-converting enzyme 2 (ACE-2) as a receptor for docking to the host cell. Essential for entry is the priming of the spike (S) protein of the virus by host cell proteases. A broadly based team led by infection biologists from the German Primate Centre and with the participation of the Charité Hospital in Berlin, the Hanover Veterinary University Foundation, the BG-UnfallklinikMurnau, the LMU Munich, the Robert Koch Institute and the German Centre for Infection Research wanted to find out how SARS-CoV-2 enters host cells and how this process can be blocked [1]. They have published their findings in the journal "Cell" [1]. The team of scientists was initially able to confirm that SARS-CoV-2 docks to the host cell via the ACE-2 receptor. They also identified Transmembrane serine protease 2 (TMPRSS2) as the cellular protein responsible for entry into the cell [1-3].

Coronavirus and Homo Sapiens in Coronavirus Disease 2019 (COVID-19)

2020 ◽  
Vol 4 (02) ◽  
pp. 121-131
Author(s):  
Pooja Natarajan ◽  
Muralidhar Kanchi ◽  
Vikneswaran Gunaseelan ◽  
Alben Sigamani ◽  
Harmon James ◽  
...  
Keyword(s):  
Viral Entry ◽  
Homo Sapiens ◽  
Influenza Pandemic ◽  
The Novel ◽  
Angiotensin Converting Enzyme 2 ◽  
Spanish Influenza ◽  
Mechanism Of Interaction ◽  
Hypoxic Respiratory Failure ◽  
Current Outbreak ◽  
Novel Coronavirus

AbstractThe Spanish influenza pandemic of 1918 globally claimed between 50 and 100 million lives. In India, it was referred to as “The Bombay Fever” and accounted for a fifth of the global death toll. The current outbreak of the novel coronavirus (2019-nCoV), a new human-infecting β-coronavirus, has clearly demonstrated that the size of an organism does not reflect on its ability to affect an entire human population. 2019-nCOV, first detected in December 2019 in Wuhan, China, spread rapidly globally. Disease in humans ranged from flulike symptoms to severe acute hypoxic respiratory failure. The virus appears closely related to two bat-derived severe acute respiratory syndromes (SARS) coronaviruses. Although bats were likely the original host, animals sold at the Huanan seafood market in Wuhan might have been the intermediate host that enabled the emergence of the virus in humans. Under the electron microscope, the SARS-CoV-2 virus grips its receptor tighter than the virus behind the SARS outbreak in 2003 to 2004. The viral particle docks onto the angiotensin-converting enzyme 2 (ACE2) receptor and initiates viral entry. This review discusses the various aspects of the SARS-CoV-2 virus, its structure, pathophysiology, mechanism of interaction with human cells, virulence factors, and drugs involved in the treatment of the disease.

scholarly journals Interplay of Opposing Effects of the WNT/β-Catenin Pathway and PPARγ and Implications for SARS-CoV2 Treatment

2021 ◽  
Vol 12 ◽  
Author(s):  
Alexandre Vallée ◽  
Yves Lecarpentier ◽  
Jean-Noël Vallée
Keyword(s):  
Distress Syndrome ◽  
The Novel ◽  
Cytokine Storm ◽  
Angiotensin Converting Enzyme 2 ◽  
Tnf Α ◽  
Pparγ Agonists ◽  
Novel Coronavirus ◽  
Opposing Effects ◽  
Canonical Wnt

The Coronavirus disease 2019 (COVID-19), caused by the novel coronavirus SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), has quickly reached pandemic proportions. Cytokine profiles observed in COVID-19 patients have revealed increased levels of IL-1β, IL-2, IL-6, and TNF-α and increased NF-κB pathway activity. Recent evidence has shown that the upregulation of the WNT/β-catenin pathway is associated with inflammation, resulting in a cytokine storm in ARDS (acute respire distress syndrome) and especially in COVID-19 patients. Several studies have shown that the WNT/β-catenin pathway interacts with PPARγ in an opposing interplay in numerous diseases. Furthermore, recent studies have highlighted the interesting role of PPARγ agonists as modulators of inflammatory and immunomodulatory drugs through the targeting of the cytokine storm in COVID-19 patients. SARS-CoV2 infection presents a decrease in the angiotensin-converting enzyme 2 (ACE2) associated with the upregulation of the WNT/β-catenin pathway. SARS-Cov2 may invade human organs besides the lungs through the expression of ACE2. Evidence has highlighted the fact that PPARγ agonists can increase ACE2 expression, suggesting a possible role for PPARγ agonists in the treatment of COVID-19. This review therefore focuses on the opposing interplay between the canonical WNT/β-catenin pathway and PPARγ in SARS-CoV2 infection and the potential beneficial role of PPARγ agonists in this context.

scholarly journals Investigation of the genetic variation in ACE2 on the structural recognition by the novel coronavirus (SARS-CoV-2)

2020 ◽  
Author(s):  
Xingyi Guo ◽  
Zhishan Chen ◽  
Yumin Xia ◽  
Weiqiang Lin ◽  
Hongzhi Li
Keyword(s):  
Genetic Variation ◽  
The Novel ◽  
S Protein ◽  
Angiotensin Converting Enzyme 2 ◽  
Missense Variants ◽  
Catalytic Metal ◽  
Using Data ◽  
Novel Coronavirus ◽  
Insight Into

Abstract Background: The outbreak of coronavirus disease (COVID-19) was caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), through its surface spike glycoprotein (S protein) recognition on the receptor Angiotensin-converting enzyme 2 (ACE2) in humans. However, it remains unclear how genetic variations in ACE2 may affect its function and structure, and consequently alter the recognition by SARS-CoV-2. Methods: We have systemically characterized missense variants in the gene ACE2 using data from the Genome Aggregation Database (gnomAD; N = 141,456). To investigate the putative deleterious role of missense variants, six existing functional prediction tools were applied to evaluate their impact. We further analyzed structural flexibility of ACE2 and the protein-protein interface with the S protein of SARS-CoV-2 using our developed Legion Interfaces Analysis (LiAn) program. Results: Here, we characterized a total of 12 ACE2 putative deleterious missense variants. Of those 12 variants, we further showed that p.His378Arg could directly weaken the binding of catalytic metal atom to decrease ACE2 activity and p.Ser19Pro could distort the most important helix to the S-protein. Another seven missense variants may affect secondary structures (i.e. p.Gly211Arg; p.Asp206Gly; p.Arg219Cys; p.Arg219His, p.Lys341Arg, p.Ile468Val, and p.Ser547Cys), whereas p.Ile468Val with AF = 0.01 is only present in Asian. Conclusions: We provide strong evidence of putative deleterious missense variants in ACE2 that are present in specific populations, which could disrupt the function and structure of ACE2. These findings provide novel insight into the genetic variation in ACE2 which may affect the SARS-CoV-2 recognition and infection, and COVID-19 susceptibility and treatment.

scholarly journals COVID-19: A Bibliometric Analysis and Insights

2020 ◽  
Vol 5 (6) ◽  
pp. 1155-1169
Author(s):  
Prerna Gautam ◽  
Sumit Maheshwari ◽  
Singh Mathuria Kaushal-Deep ◽  
Abdul Rashid Bhat ◽  
Chandra K. Jaggi
Keyword(s):  
State Of The Art ◽  
Human Life ◽  
Time Frame ◽  
The Novel ◽  
Ongoing Research ◽  
Current Trends ◽  
Current Outbreak ◽  
Novel Coronavirus ◽  
Work Done

The current outbreak of the coronavirus disease has left the whole world traumatised. The illness triggered by the novel coronavirus is named as COVID-19. It is pre-fixed with the word “novel” because it comes under the new strain of the virus that has not been reported before. This virus outbreak has disrupted human life in the most petrifying way worldwide. The present study aims to analyse the work done in this field through a state-of-the-art review of articles based on COVID-19 and discuss the current trends in the epidemiology of this disease entity with special reference to India and the effects of this pandemic on the environment. The time frame selected for review is the beginning of this pandemic to April 10th, 2020. Scopus® database is used to carry out the analysis. Moreover, the most contributed authors, institutions, countries, etc. are showed through the analysis. The purpose of this review is to get an idea about the direction of the flow of current research, the association of various authors with each other, the role of collaboration between several institutions and the position of India in current explosive ongoing research.

scholarly journals Coronavirus and Homo Sapiens

2020 ◽  
Author(s):  
Pooja Natarajan ◽  
Muralidhar Kanchi ◽  
Vikneswaran Gunaseelan ◽  
Alben Sigamani ◽  
James Harmon ◽  
...  
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Viral Entry ◽  
Homo Sapiens ◽  
Influenza Pandemic ◽  
The Novel ◽  
Angiotensin Converting Enzyme 2 ◽  
Mechanism Of Interaction ◽  
Hypoxic Respiratory Failure ◽  
Current Outbreak ◽  
Novel Coronavirus

AbstractThe Spanish influenza pandemic of 1918 globally claimed death between 50 and 100 million lives. In India, it was referred to as “The Bombay Fever,” and accounted for a fifth of the global death toll at that time. The current outbreak of the novel coronavirus disease 2019 (COVID-19), a new human-infecting beta coronavirus, has demonstrated that the size of an organism does not reflect on its ability to affect almost an entire human population. COVID-19, first detected in December 2019 in Wuhan, China, that spread rapidly worldwide. In humans, this disease ranged from flu-like symptoms to severe acute hypoxic respiratory failure. By appearance, this virus closely related to two bat-derived severe acute respiratory syndrome (SARS) coronaviruses. Although bats were likely the original host, animals sold at the Huanan seafood market in Wuhan might have been the intermediate host that enabled the emergence of the virus in humans. Under the electron microscope, the severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) virus grips its receptor tighter than the virus behind the SARS outbreak in 2003 to 2004. The viral particle docks onto the angiotensin-converting enzyme 2 (ACE2) receptor and initiates viral entry. This review discusses the various aspects of the SARS-CoV-2 virus, its structure, pathophysiology, mechanism of interaction with human cells, virulence factors, and drug involved in the treatment of the disease.

scholarly journals COVID-19 in Children: Do They Have a Lower Risk of Severe Infection Than Adults?

2021 ◽  
Vol 12 (3) ◽  
Author(s):  
Mohammad Reza Amiri
Keyword(s):  
Health Resources ◽  
Severe Infection ◽  
Severe Form ◽  
The Novel ◽  
Angiotensin Converting Enzyme 2 ◽  
Pediatric Populations ◽  
Limited Health ◽  
Novel Coronavirus ◽  
Infants And Young Children

: The novel coronavirus disease 2019 (COVID-19), which was first identified in Wuhan, China, in late 2019, has now spread around the world. It significantly affects the lower respiratory tract, and pneumonia is always present in patients with the severe form of the disease. Many studies have shown that the severity of COVID-19 is lower in pediatric populations. It is important to determine why infants and young children are not severely affected by COVID-19. By increasing our awareness of this disease, we can prioritize our limited health resources. Several theories have been proposed to explain such significant differences between the pediatric and adult populations with COVID-19. Some of them are: (1) the role of angiotensin-converting enzyme 2 (ACE2); (2) cross-immunity with other severe acute respiratory syndrome (SARS)-like viruses; (3) obtunded systemic inflammatory response in children; (4) more efficient T cells in them; (5) interactions of SARS-Coronavirus-2 (SARS-CoV-2) with other viruses in the mucosa of the lungs and airways; and (6) a hypothesis that COVID-19 proteins onslaught the heme on the β-1 chain of hemoglobin. The important thing to keep in mind is that the asymptomatic and mildly symptomatic pediatrics are crucial in the spread of COVID-19.

scholarly journals A Review on Catastrophic Evolution of SARS-CoV to SARS-CoV2-A Global Pandemic

Coronaviruses ◽  
2020 ◽  
Vol 01 ◽  
Author(s):  
Sushmita Krishnan ◽  
Darshini Subramanian ◽  
Sri Sakthi Priyadarshini Rajamani
Keyword(s):  
The Novel ◽  
Angiotensin Converting Enzyme 2 ◽  
Global Pandemic ◽  
The Family ◽  
Natural Hosts ◽  
Current Outbreak ◽  
Global Statistics ◽  
Novel Coronavirus ◽  
And Control ◽  
Alternative Drugs

: The coronaviruses belonging to the family Coronaviridae have caused a massive pandemic in December 2019 af-ter its previous outbreaks as SARS-CoV and MERS. The outbreak is believed to have originated from the seafood and live market in Hubei province of China. The Rhinolophus species are the natural hosts of this virus. The unknown virus caus-ing pneumonia took away so many lives before recognising it as the novel Coronavirus. Very little information is known about the biology and nature of the current outbreak. This article reviews multiple aspects encompassing its origin, epide-miology, pathogenesis, symptoms and the global statistics of spread. Acute respiratory distress syndrome (ARDS) is the key symptom of this condition. Angiotensin converting enzyme 2 (ACE2) helps in the penetration of the virus into the tar-get cells. Deeper research and understanding is essential for identification of antibodies that inhibit ACE2 and can prevent viral replication. Drug design and control of disease is crucial. In countries like India where plant diversity is extensive, it is wise to focus on plant based alternative drugs. Many attempts have been made to review and curate the drug discovery attempts using immune-informatics and bioinformatics tools.

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