scholarly journals SARS-CoV-2 host cell entry might involve Beta adrenergic receptors

2020 ◽  
Author(s):  
Vasanthakumar Natesan
Keyword(s):  
Host Cell ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Cell Receptor ◽  
Cell Entry ◽  
Beta Adrenergic ◽  
Angiotensin Converting Enzyme 2 ◽  
Host Cell Receptor ◽  
Host Cell Entry ◽  
Cluster Of Differentiation

Coronavirus disease 2019 (COVID-19) is caused by Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. SARS-CoV-2 enters the host cell by binding its spike protein with the angiotensin-converting enzyme 2 (ACE2) receptor. Cluster of differentiation 147 (CD147) also known as Basigin or extracellular matrix metalloproteinase inducer (EMMPRIN), has been proposed as another host cell receptor that might be involved in SARS-CoV-2 cellular entry . Any other host cell receptors that exist for SARS-CoV-2 is not known at present. I suggest that the Beta adrenergic receptor might be involved in the SARS-CoV-2 cell entry, and act as a co-receptor by its interaction via surface vimentin to the ACE2 receptor and by forming a complex with CD147.

scholarly journals Computational insights into differential interaction of mamalian ACE2 with the SARS-CoV-2 spike receptor binding domain

2021 ◽  
Author(s):  
Cecylia S. Lupala ◽  
Vikash Kumar ◽  
Xiao-dong Su ◽  
Chun Wu ◽  
Haiguang Liu
Keyword(s):  
Receptor Binding ◽  
Cell Receptor ◽  
Binding Domain ◽  
Cell Entry ◽  
Receptor Binding Domain ◽  
Sequence Structure ◽  
Angiotensin Converting Enzyme 2 ◽  
Host Cell Receptor ◽  
Comparison Results ◽  
Horseshoe Bat

AbstractThe severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causing agent of the COVID-19 pandemic, has spread globally. Angiotensin-converting enzyme 2 (ACE2) has been identified as the host cell receptor that binds to receptor-binding domain (RBD) of the SARS-COV-2 spike protein and mediates cell entry. Because the ACE2 proteins are widely available in mammals, it is important to investigate the interactions between the RBD and the ACE2 of other mammals. Here we analyzed the sequences of ACE2 proteins from 16 mammals and predicted the structures of ACE2-RBD complexes. Analyses on sequence, structure, and dynamics synergistically provide valuable insights into the interactions between ACE2 and RBD. The comparison results suggest that the ACE2 of bovine, cat and panda form strong binding with RBD, while in the cases of rat, least horseshoe bat, horse, pig, mouse and civet, the ACE2 proteins interact weakly with RBD.

scholarly journals Host-cell recognition through GRP78 is enhanced in the new variants of SARS-CoV-2; in silico perspective

2021 ◽  
Author(s):  
Abdo Elfiky ◽  
Ibrahim M Ibrahim ◽  
Alaa M Elgohary
Keyword(s):  
Cell Surface ◽  
Host Cell ◽  
South African ◽  
Cell Receptor ◽  
Binding Motif ◽  
Angiotensin Converting Enzyme 2 ◽  
Host Cell Receptor ◽  
Binding Surface ◽  
New Variant ◽  
The Uk

Abstract New SARS-CoV-2 variants started in the UK and South Africa in December 2020 and currently spreading worldwide during the last few days. Additionally, another more recent variant sparked in Brazil (B.1.1.248 lineage) this month. The new variant 501.V2 (South African) bears three mutations in the receptor-binding domain (RBD) of the spike glycoprotein, K417N, E484K, and N501Y, while the Brazilian B.1.1.248 lineage have 12 mutations. The N501Y mutation is found in South African and Brazilian variants and is also shared with the UK variant VOC-202012/01 (1). This mutation may affect the host-cell receptor ACE2 (angiotensin-converting enzyme 2) recognition (2). Despite its presence in the ACE2 binding surface, we showed that the N501Y mutant shows a remarkable increase in binding of the ACE2-RBD complex to the host-cell surface Glucose Regulated Protein 78 (CS-GRP78) (3). On the other hand, the E484K is found in the spike RBD's binding motif that we reported earlier to be recognized by cell-surface GRP78 (C480-C488 region of the spike) (4). In this study, we simulate the complex ACE2-SARS-CoV-2 spike RBD system in which the RBD is in the wildtype and mutated (K417N, E484K, and N501Y) isoforms. Additionally, the CS-GRP78 association with the ACE2-SARS-CoV-2 spike RBD complex (ACE2-RBD) is modeled at the presence of these mutant variants of the viral spike.

Understanding the Role of Corona Virus based on Current Scientific Evidence - A Review with Emerging Importance in Pandemic

2020 ◽  
Vol 15 (2) ◽  
pp. 89-103
Author(s):  
Suman K. Ray ◽  
Sukhes Mukherjee
Keyword(s):  
Host Cell ◽  
Scientific Evidence ◽  
Antibody Therapy ◽  
Cell Receptor ◽  
Spike Protein ◽  
Virus Infectivity ◽  
Angiotensin Converting Enzyme 2 ◽  
Host Cell Receptor ◽  
Antiviral Medications

: Coronavirus disease is a potentially deadly disease and of significant apprehension for global communal health because of its lethality. Vaccines and antiviral medications are still under trial to prevent or treat human coronavirus (HCoV) till date. The virus HCoV originated in 2003, SARS-CoV, which causes respiratory syndrome having distinctive pathogenesis and infections of the respiratory tract. A mechanism was projected for the evolution of SARS virus, and a handy association with bats was found. When this virus reaches the respective host system, the infection starts with spike protein binding to its complementary receptor of the host cell. The coronavirus spike protein’s association with its host cell receptor complement is crucial in deciding the virus infectivity, tissue tropism and species variety. Recent studies show that SARS Coronavirus 2 or COVID-19 requires protease to get into cells, offering a new therapeutic target. Distinctive attention and exertions should be given to defending or reducing transmission in vulnerable populaces, including those directly associated with caregiving and treatment and also aged one. Researchers are planning to develop a vaccine for COVID-19, and in this approach are also considered developing a vaccine that sensitizes our immune system preventing from this pandemic. The present review focuses on the role of S-spike protein in COVID-19, which helps the virus intruding the enzyme ACE2 (Angiotensin-Converting Enzyme 2). Passive antibody therapy is an additional alternative to use blood donors from hale and hearty people who have already recovered from COVID-19 and therapeutic advancement in handling the COVID-19 pandemic.

scholarly journals Antcins from Antrodia cinnamomea and Antrodia salmonea Inhibit Angiotensin-Converting Enzyme 2 (ACE2) in Epithelial Cells: Can Be Potential Candidates for the Development of SARS-CoV-2 Prophylactic Agents

Plants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1736
Author(s):  
K. J. Senthil Kumar ◽  
M. Gokila Vani ◽  
Han-Wen Hsieh ◽  
Chin-Chung Lin ◽  
Sheng-Yang Wang
Keyword(s):  
Epithelial Cells ◽  
Angiotensin Converting Enzyme ◽  
Host Cell ◽  
Disease Onset ◽  
Cell Entry ◽  
Converting Enzyme ◽  
Medicinal Mushrooms ◽  
Angiotensin Converting Enzyme 2 ◽  
Antrodia Cinnamomea ◽  
Host Cell Entry

Antcins are newly identified steroid-like compounds from Taiwan’s endemic medicinal mushrooms Antrodia cinnamomea and Antrodia salmonea. Scientific studies of the past two decades confirmed that antcins have various pharmacological activities, including potent anti-oxidant and anti-inflammatory effects. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused the coronavirus disease-2019 (COVID-19) pandemic and is characterized as a significant threat to global public health. It was recently identified that SARS-CoV-2 required angiotensin converting enzyme 2 (ACE2), a receptor which supports host cell entry and disease onset. Here, we report a novel function of antcins, in which antcins exhibit inhibitory effects on ACE2. Compared to the untreated control group, treatment with various antcins (antcin-A, antcin-B, antcin-C, antcin-H, antcin-I, and antcin-M) significantly inhibited ACE2 activity in cultured human epithelial cells. Indeed, among the investigated antcins, antcin-A, antcin-B, antcin-C, and antcin-I showed a pronounceable inhibition against ACE2. These findings suggest that antcins could be novel anti-ACE2 agents to prevent SARS-CoV-2 host cell entry and the following disease onset.

scholarly journals Understanding SARS-CoV-2 features of infectivity, aggressiveness, and transmissibility: an insect-vector theory for SARS-CoV-2 dissemination

2021 ◽  
Vol 4 (Special1) ◽  
pp. 343-347
Author(s):  
Angela Madalina Lazar
Keyword(s):  
Host Cell ◽  
Cell Entry ◽  
Virus Infectivity ◽  
Insect Vector ◽  
Multiple Forms ◽  
Tissue Destruction ◽  
Angiotensin Converting Enzyme 2 ◽  
Infectivity Rate ◽  
Vector Theory ◽  
Host Cell Entry

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a ribonucleic acid–based (RNA-based) lineage B β-coronavirus characterized by 10-20 times higher infectivity and transmissibility even across species than previous coronaviruses. The significant infectivity rate of SARS-CoV-2 is due to its different host cell entry mechanisms that are mainly via angiotensin-converting enzyme 2 (ACE2) receptors contrasting earlier coronaviruses that used mainly the endosomal route. Due to the widespread distribution of ACE2 receptors throughout our body, various routes of infectivity are possible, highlighting the necessity of employing multiple forms of protection besides face masks to limit inter-human transmissibility. SARS-CoV-2 exhibits other remarkable features such as the ability to escape the immune system repeated genomic mutations that make it difficult to design a vaccine to address all viral strains and form huge host cell syncytia leading to massive tissue destruction. If we accept SARS-CoV-2 primary reservoir from bats, we should investigate the routes of viral inter-species propagation. In this article, a new theory is proposed- that the dissemination of the virus from the bats to other species and humans could have been possible via an insect vector, as insects possess significant amounts of both ACE2 receptors and a disintegrin and metalloprotease 17 (ADAM-17) enzymes that are essential for virus infectivity. .

COVID 19 – Eye Issues

2020 ◽  
Vol 5 (Special) ◽  
Keyword(s):  
Host Cell ◽  
Target Cell ◽  
Cell Receptor ◽  
Human Tissues ◽  
Type Ii ◽  
Cell Infection ◽  
Host Cell Receptor ◽  
Infected Cells ◽  
Cellular Entry

The coronavirus illness (COVID-19) is caused by a new recombinant SARS-CoV (SARS-CoV) virus (SARS-CoV-2). Target cell infection by SARS-CoV is mediated by the prickly protein of the coronavirus and host cell receptor, enzyme 2 converting angiotensin (ACE2) [3]. Similarly, a recent study suggests that cellular entry by SARS-CoV-2 is dependent on both ACE2 as well as type II transmembrane axial protease (TMPRSS2) [4]. This means that detection of ACE2 and PRSS2 expression in human tissues can predict potential infected cells and their respective effects in COVID-19 patients [1].

scholarly journals Overexpression of beta-arrestin and beta-adrenergic receptor kinase augment desensitization of beta 2-adrenergic receptors.

1993 ◽  
Vol 268 (5) ◽  
pp. 3201-3208
Author(s):  
S. Pippig ◽  
S. Andexinger ◽  
K. Daniel ◽  
M. Puzicha ◽  
M.G. Caron ◽  
...  
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Receptor Kinase ◽  
Beta Adrenergic Receptor ◽  
Beta Adrenergic ◽  
Beta 2
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