scholarly journals An Overview On Transmission Of Diseases In Special Reference To COVID-19 And Potential Targets To Control This Pandemic

2020 ◽  
Vol 4 (1) ◽  
pp. 1-6
Author(s):  
Vibha Yadav ◽  
Keyword(s):  
Rna Virus ◽  
Close Contact ◽  
Adaptive Immune Response ◽  
Cell Receptor ◽  
Angiotensin Converting Enzyme 2 ◽  
Infected People ◽  
Adaptive Immune ◽  
Host Cell Receptor ◽  
Positive Sense ◽  
Respiratory Droplets

With its initial outbreak in China, the virus was referred as "coronavirus". WHO has named it "severe acute respiratory syndrome coronavirus 2" (SARS-CoV-2). It has been described as the successor to SARS-CoV-1 which is a positive-sense single-stranded RNA virus. The virus spreads mainly between people who are in close contact (less than two metres or six feet) through small droplets produced during coughing, sneezing, or talking. Infected people exhale the contaminated droplets which are then inhaled into the lungs, or settle on other non- infected people's faces his/her mucosae (mouth and nose) or conjunctiva (eyes) get exposed to potentially infective respiratory droplets to cause new infection. Organism may enter to human cells by binding to the receptor angiotensin converting enzyme 2 (ACE2). Research works are in progress to find potential targets to control the pandemic. To control and treat the virus various targets are under study and these targets range from modulating host cell receptor for the virus entry to generate an effective adaptive immune response.

An overview on transmission of diseases in special reference to COVID-19 and potential targets to control this pandemic

2020 ◽  
pp. 05-14
Author(s):  
Vibha Yadav ◽  
Mrigendra Rajput ◽  
Diwakar R.P ◽  
Rajesh Kumar
Keyword(s):  
Rna Virus ◽  
Close Contact ◽  
Adaptive Immune Response ◽  
Cell Receptor ◽  
Angiotensin Converting Enzyme 2 ◽  
Infected People ◽  
Adaptive Immune ◽  
Host Cell Receptor ◽  
Positive Sense ◽  
Respiratory Droplets

With its initial outbreak in China, the virus was referred as "coronavirus". WHO has named it "severe acute respiratory syndrome coronavirus 2" (SARS-CoV-2). It has been described as the successor to SARS-CoV-1which is a positive-sense single-stranded RNA virus. The virus spreads mainly between people who are in close contact (less than two metres or six feet) through small droplets produced during coughing, sneezing, or talking. Infected people exhale the contaminated droplets which are then inhaled into the lungs, or settle on other non- infected people's faces his/her mucosae (mouth and nose) or conjunctiva (eyes) get exposed to potentially infective respiratory droplets to cause new infection. It mainly enters human cells by binding to the receptor angiotensin converting enzyme 2 (ACE2). Research works are in progress to find potential targets to control the pandemic. To control and treat the virus various targets are under study and these targets range from modulating host cell receptor for the virus entry to generate an effective adaptive immune response.

Herbal Medicine in Fighting Against COVID-19: New Battle with an Old Weapon

2021 ◽  
Vol 22 ◽  
Author(s):  
Ranjit K. Harwansh ◽  
Shiv Bahadur
Keyword(s):  
Herbal Medicine ◽  
Rna Virus ◽  
Plant Secondary Metabolites ◽  
Cell Receptor ◽  
Inhibitory Effect ◽  
World Population ◽  
Main Process ◽  
Potential Health ◽  
Host Cell Receptor ◽  
Novel Coronavirus

: World population has been suffering due to the outbreak of present pandemic situation of COVID-19. The disease has become life-threatening in a very short time with touching on most of the citizenry and economic systems globally. The novel virus, SARS-CoV-2 has been known as the causative agent of COVID-19. The SARS-CoV-2 is single stranded RNA virus having ~30 kb genomic components which are 70% identical to SARS-CoV. The main process of pathophysiology of COVID-19 has been associated with the interaction of a novel coronavirus with host cell receptor, angiotensin-converting enzyme-2 (ACE 2) by fusion. Therapeutic agents having serine protease inhibitors and ACE-2 blockers may be explored for the treatment by inhibiting the viral target such as Mpro, RdRp, PLpro and helicase. Herbal medicine has a wide array chemical entity with potential health benefits including antiviral activity which may be explored as alternative treatment of COVID-19. The herbal bioactives like catechins, andrographolide, hesperidin, biorobin, scutellarein, silvestrol, shikonin, tryptanthrin, vitexin quercetin, myricetin, caffeic acid, psoralidin, luteolin etc have showed potential inhibitory effect against SARS-CoV-2. Recent research reports indicate that the various plant secondary metabolites have shown the potential antiviral activities. The present review article highlights on the recent information on the mechanism of actions and applications of herbal medicine in the treatment of COVID-19.

scholarly journals An ultrapotent synthetic nanobody neutralizes SARS-CoV-2 by stabilizing inactive Spike

Science ◽  
2020 ◽  
pp. eabe3255 ◽  
Author(s):  
Michael Schoof ◽  
Bryan Faust ◽  
Reuben A. Saunders ◽  
Smriti Sangwan ◽  
Veronica Rezelj ◽  
...  
Keyword(s):  
Cell Receptor ◽  
Affinity Maturation ◽  
Host Cells ◽  
Spike Protein ◽  
Airway Epithelia ◽  
Angiotensin Converting Enzyme 2 ◽  
Inactive Conformation ◽  
Binding Domains ◽  
Host Cell Receptor ◽  
Yeast Surface

The SARS-CoV-2 virus enters host cells via an interaction between its Spike protein and the host cell receptor angiotensin converting enzyme 2 (ACE2). By screening a yeast surface-displayed library of synthetic nanobody sequences, we developed nanobodies that disrupt the interaction between Spike and ACE2. Cryogenic electron microscopy (cryo-EM) revealed that one nanobody, Nb6, binds Spike in a fully inactive conformation with its receptor binding domains (RBDs) locked into their inaccessible down-state, incapable of binding ACE2. Affinity maturation and structure-guided design of multivalency yielded a trivalent nanobody, mNb6-tri, with femtomolar affinity for Spike and picomolar neutralization of SARS-CoV-2 infection. mNb6-tri retains function after aerosolization, lyophilization, and heat treatment, which enables aerosol-mediated delivery of this potent neutralizer directly to the airway epithelia.

scholarly journals Geranium and Lemon Essential Oils and Their Active Compounds Downregulate Angiotensin-Converting Enzyme 2 (ACE2), a SARS-CoV-2 Spike Receptor-Binding Domain, in Epithelial Cells

Plants ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 770 ◽  
Author(s):  
K. J. Senthil Kumar ◽  
M. Gokila Vani ◽  
Chung-Shuan Wang ◽  
Chia-Chi Chen ◽  
Yu-Chien Chen ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Angiotensin Converting Enzyme ◽  
Essential Oils ◽  
Cell Receptor ◽  
Gas Chromatography Mass Spectrometry ◽  
Converting Enzyme ◽  
Inhibitory Effects ◽  
Angiotensin Converting Enzyme 2 ◽  
Host Cell Receptor ◽  
Lemon Oil

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), also known as coronavirus disease-2019 (COVID-19), is a pandemic disease that has been declared as modern history’s gravest health emergency worldwide. Until now, no precise treatment modality has been developed. The angiotensin-converting enzyme 2 (ACE2) receptor, a host cell receptor, has been found to play a crucial role in virus cell entry; therefore, ACE2 blockers can be a potential target for anti-viral intervention. In this study, we evaluated the ACE2 inhibitory effects of 10 essential oils. Among them, geranium and lemon oils displayed significant ACE2 inhibitory effects in epithelial cells. In addition, immunoblotting and qPCR analysis also confirmed that geranium and lemon oils possess potent ACE2 inhibitory effects. Furthermore, the gas chromatography-mass spectrometry (GC–MS) analysis displayed 22 compounds in geranium oil and 9 compounds in lemon oil. Citronellol, geraniol, and neryl acetate were the major compounds of geranium oil and limonene that represented major compound of lemon oil. Next, we found that treatment with citronellol and limonene significantly downregulated ACE2 expression in epithelial cells. The results suggest that geranium and lemon essential oils and their derivative compounds are valuable natural anti-viral agents that may contribute to the prevention of the invasion of SARS-CoV-2/COVID-19 into the human body.

scholarly journals Characterisation of a novel ACE2-based therapeutic with enhanced rather than reduced activity against SARS-CoV-2 variants.

2021 ◽  
Author(s):  
Mathieu Ferrari ◽  
Leila Mekkaoui ◽  
F. Tudor Ilca ◽  
Zulaikha Akbar ◽  
Reyisa Bughda ◽  
...  
Keyword(s):  
Viral Infections ◽  
Scale Up ◽  
Renin Angiotensin System ◽  
Cell Receptor ◽  
Biophysical Properties ◽  
Angiotensin Converting Enzyme 2 ◽  
Host Cell Receptor ◽  
System 2 ◽  
Reduced Activity ◽  
Reduced Risk

The human angiotensin-converting enzyme 2 acts as the host cell receptor for SARS-CoV-2 and the other members of the Coronaviridae family SARS-CoV-1 and HCoV-NL63. Here we report the biophysical properties of the SARS-CoV-2 spike variants D614G, B.1.1.7, B.1.351 and P.1 with affinities to the ACE2 receptor and infectivity capacity, revealing weaknesses in the developed neutralising antibody approaches. Furthermore, we report a pre-clinical characterisation package for a soluble receptor decoy engineered to be catalytically inactive and immunologically inert, with broad neutralisation capacity, that represents an attractive therapeutic alternative in light of the mutational landscape of COVID-19. This construct efficiently neutralised four SARS-CoV-2 variants of concern. The decoy also displays antibody-like biophysical properties and manufacturability, strengthening its suitability as a first-line treatment option in prophylaxis or therapeutic regimens for COVID-19 and related viral infections. IMPORTANCE Mutational drift of SARS-CoV-2 risks rendering both therapeutics and vaccines less effective. Receptor decoy strategies utilising soluble human ACE2 may overcome the risk of viral mutational escape since mutations disrupting viral interaction with the ACE2 decoy will by necessity decrease virulence thereby preventing meaningful escape. The solution described here of a soluble ACE2 receptor decoy is significant for the following reasons: While previous ACE2-based therapeutics have been described, ours has novel features including (1) mutations within ACE2 to remove catalytical activity and systemic interference with the renin/angiotensin system; (2) abrogated FcγR engagement, reduced risk of antibody-dependent enhancement of infection and reduced risk of hyperinflammation, and (3) streamlined antibody-like purification process and scale-up manufacturability indicating that this receptor decoy could be produced quickly and easily at scale. Finally, we demonstrate that ACE2-based therapeutics confer a broad-spectrum neutralisation potency for ACE2-tropic viruses, including SARS-CoV-2 variants of concern in contrast to therapeutic mAb.

scholarly journals Immune Response to COVID-19

2021 ◽  
Author(s):  
Ricardo Wesley Alberca
Keyword(s):  
Immune Response ◽  
Adaptive Immune Response ◽  
Multiple Organ ◽  
Disease Course ◽  
Angiotensin Converting Enzyme 2 ◽  
Damage And Failure ◽  
Adaptive Immune ◽  
General Aspects ◽  
Inflammatory Molecules ◽  
The Impact

The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) invades the host’s cells via the angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2). ACE2 and TMPRSS2 molecules are highly expressed on the respiratory tract but are also expressed in other organs such as kidneys, heart, and intestine, which could partially explain the multiple organ infection, damage, and failure. During the COVID-19 disease course, patients may develop a dysregulation in the immune response, with an exacerbated production of pro-inflammatory molecules and hypercoagulation, which can collaborate to the increase in tissue damage and death. This chapter will cover general aspects of the innate and adaptive immune response during COVID-19, the impact of comorbidities on the immune response to SARS-CoV-2, and the immune response generated by COVID-19 vaccines.

scholarly journals The Dynamics of Innate and Adaptive Immune Response to Sars Cov-2 Infection and Its Limitations in Human Beings

2021 ◽  
pp. 10-25
Author(s):  
Akpanda Etido ◽  
Emmanuel Ifeanyi Obeagu ◽  
Chukwuma J. Okafor ◽  
Udunma Olive Chijioke ◽  
C. C. N. Vincent ◽  
...  
Keyword(s):  
Immune Response ◽  
Severe Acute Respiratory Syndrome ◽  
Interleukin 1 ◽  
Adaptive Immune Response ◽  
Infection Process ◽  
Host Cells ◽  
Human Beings ◽  
Infected People ◽  
Adaptive Immune ◽  
Cell Immunity

This article deals with the dynamics of the innate and adaptive immune response to severe acute respiratory syndrome coronavirus 2 (SARSCoV2) infection. SARSCoV2 is the viral factor that causes the current global coronavirus pandemic disease 2019 (COVID2019). In terms of person-to-person transmission, it is contacted by inhaling the sneeze droplets of infected people. Severe acute respiratory syndrome Coronavirus 2 attacks lung cells first in its binding mechanism because there are many conservative receptor entries, such as angiotensin converting enzyme 2. The presence of this virus in host cells triggers a variety of protective immune responses, resulting in leads to pneumonia and acute respiratory distress syndrome. In the SarsCoV2 infection process, virus replication, immune response, and inflammatory response are dynamic events that can change rapidly; leading to different results, involving the dynamic expression of pro-inflammatory genes, peaking after the lowest point of respiratory function and leading to a cytokine storm, research on the interleukin 1 (IL1) pathway has shown that it is a factor related in severe respiratory diseases. The weakened expression of cytokines associated with mild infections will also delay T cell immunity to SARSCoV2, thereby prolonging the infection time; this indicates that such afebrile (afebrile) infections and undifferentiated COVID19 cases may promote the virus in the community Spread. This review aims to provide a general overview of the dynamics involved in the human immune response to this viral infection. It also includes a brief description of its structure, discovery history and pathogenesis to facilitate the understanding of this article.

scholarly journals Increasing Host Cellular Receptor—Angiotensin-Converting Enzyme 2 (ACE2) Expression by Coronavirus may Facilitate 2019-nCoV Infection

2020 ◽  
Author(s):  
Pei-Hui Wang ◽  
Yun Cheng
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Emerging Infectious Diseases ◽  
Cell Receptor ◽  
Host Cells ◽  
Cellular Receptor ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Host Cell Receptor ◽  
Coronavirus Infection ◽  
Entry Receptor

AbstractThe ongoing outbreak of a new coronavirus (2019-nCoV) causes an epidemic of acute respiratory syndrome in humans. 2019-nCoV rapidly spread to national regions and multiple other countries, thus, pose a serious threat to public health. Recent studies show that spike (S) proteins of 2019-nCoV and SARS-CoV may use the same host cell receptor called angiotensin-converting enzyme 2 (ACE2) for entering into host cells. The affinity between ACE2 and 2019-nCoV S is much higher than ACE2 binding to SARS-CoV S protein, explaining that why 2019-nCoV seems to be more readily transmitted from the human to human. Here, we reported that ACE2 can be significantly upregulated after infection of various viruses including SARS-CoV and MERS-CoV. Basing on findings here, we propose that coronavirus infection can positively induce its cellular entry receptor to accelerate their replication and spread, thus drugs targeting ACE2 expression may be prepared for the future emerging infectious diseases caused by this cluster of viruses.

scholarly journals Can ChAdOx1, a replication-deficient adenoviral (Ad) vector used to deliver SARS-Cov2 spike protein as a vaccine, recombine with the homologous human Ad to generate a novel Ad+Spike virus?

2020 ◽  
Author(s):  
Sandeep Chakraborty
Keyword(s):  
Viral Vector ◽  
Rna Virus ◽  
Human Adenovirus ◽  
Cell Receptor ◽  
Spike Protein ◽  
Transcriptional Unit ◽  
Human Virus ◽  
Dna And Rna ◽  
Host Cell Receptor ◽  
Weakened Version

The development of a vaccine for Covid19 is being expedited [1]. The underlying technology for the vaccines are varied: ‘nucleic acid (DNA and RNA), virus-like particle, peptide, viral vector (replicating and non- replicating), recombinant protein, live attenuated virus and inactivated virus’ [2]. Among these, ChAdOx1, a genetically modified, weakened version of a common cold virus (adenovirus) is now in human clinical trials [3]. The ChAd vector (Chimpanzee adenovirus) was introduced in 2012 Chimpanzee adenovirus Y25 [4]. A large proportion of human adults possess significant titres of neutralising antibodies to human Adv, hence the requirement for a different adenovirus. The deletion of a single transcriptional unit, E1, ensures these viruses cant replicate. Other genes like the E3 region may also be deleted. Now, in the Covid19 vaccine ChAdOx1, the spike protein gene from MERS-CoV strain Camel/Qatar/2/2014 ‘was inserted into the E1 locus of a genomic clone of ChAdOx1 using site-specific recombination’ [5].One of the theories about the genesis of SARS-Cov2 is recombination with coronaviruses from pan- golins [6]. Whether or not it happened in SARS-Cov2, there is no denying that such recombinations do happen.How do we know that the spike protein wont be inserted into a human adenovirus using recombination?Human adenovirus shares 95% homology to ChAd. The spike protein may be inserted after the E1 protein in a viable human virus. What will happen after that to the virus is anyone’s guess. Note, that there is precedence for such recombinant adenoviruses - using ‘ping-pong” zoonosis and anthroponosis’, where the genome of a promiscuous pathogen is ‘embedded with evidence of unprecedented multiple, multidirectional, stable, and reciprocal cross-species infections of hosts from three species (human, chimpanzee, and bonobo)’ [7].Another critique - co-stimulation in host cellsA spike protein from SARS-Cov2, which is supposed to bind to ACE2 and CD147 [8], has been inserted in an adenovirus. The adenovirus has its own host-cell receptor preferences [9] - what will be the consequences of co-stimulation in those cells in which both these receptors are expressed?

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.

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