Pomegranate has been traditionally used for thousands of years to treat various diseases. It contains powerful antioxidants and anti-inflammatory compounds that may help attenuate SARS-CoV-2 and its clinical outcomes. Specifically, pomegranate polyphenols can inhibit the three main mechanisms SARS-CoV-2 uses to enter host cells, as well as reduce viral replication, modulate the inflammatory response to prevent acute respiratory distress syndrome (ARDS), and induce apoptosis of infected cells. Due to these diverse mechanisms of action, pomegranate may be an effective natural therapy for managing COVID-19 infections and reducing mortality.
Coronaviruses are enveloped viruses with positive-stranded RNA genomes that encode structural and accessory proteins. SARS-CoV-2 enters cells by binding to the ACE2 receptor, and its RNA genome is then translated and replicated to produce more viral proteins and RNA. Assembly and release of new virus particles occurs in the ER and Golgi. The virus can trigger a cytokine storm involving overproduction of IL-6 that may lead to severe immune response and multi-organ dysfunction in some patients.
HCV was discovered in 1989 as a major cause of non-A, non-B hepatitis. It is a single stranded RNA virus of the Flaviviridae family. An estimated 130-170 million people worldwide are chronically infected, making it a significant global health burden.
HCV has an enveloped virion that is 50-80 nm in diameter with E1 and E2 glycoprotein spikes. Its positive-sense single stranded RNA genome is translated into a polyprotein that is cleaved into structural and non-structural proteins. The non-structural proteins NS3, NS4, NS5B are involved in replication and assembly of new virions.
Older treatments for HCV involved peg
Presentation on covide19 and used drug machanismGauriShankar38
SARS-CoV-2 is a betacoronavirus that causes COVID-19. It contains four structural proteins - envelope, spike, membrane, and nucleocapsid. The spike protein binds to the human ACE2 receptor, allowing viral entry. Remdesivir is an antiviral medication used to treat COVID-19. It works by inhibiting the SARS-CoV-2 RNA-dependent RNA polymerase, preventing viral replication. Common side effects include liver and kidney problems. Chloroquine and hydroxychloroquine are also used, and may work by interfering with glycosylation of ACE2 and viral fusion in endosomes.
SARS-CoV-2 and Covid-19: Genetics, Treatment and VaccinesDenish Aloo
The document provides information on SARS-CoV-2 and COVID-19. It discusses the history of past respiratory disease pandemics. It defines coronaviruses and SARS-CoV-2, the virus that causes COVID-19. It describes the taxonomy, structure, genome organization, mutations, and life cycle of SARS-CoV-2. It also discusses the non-structural proteins, structural proteins, and accessory proteins of SARS-CoV-2.
1) SARS-CoV is a coronavirus that emerged in 2002 causing a global pandemic. Its pathogenesis involves aberrant host innate immune responses and viral antagonism of interferon signaling.
2) Models of SARS-CoV infection like human airway epithelial cultures and mouse-adapted SARS-CoV have provided insights into innate immune pathways important for controlling SARS-CoV disease.
3) SARS-CoV encodes several proteins that antagonize type I interferon induction and signaling to evade the host innate immune response, which is an important factor in SARS pathogenesis.
Interferons are glycoproteins that are produced in response to viral infections and other pathogens in order to activate the immune system. There are three main classes of interferons - alpha, beta, and gamma - which signal through different cell surface receptor complexes. Interferons have a variety of antiviral, antitumor, and immunomodulatory properties. They are currently used clinically to treat hepatitis C virus, hepatitis B virus, multiple sclerosis, and some cancers, though their mechanisms of action are still not fully understood. Research on interferons has contributed significantly to the development of molecular biology and our understanding of cytokines.
SARS-CoV-2 has a large RNA genome that it uses to hijack the host cell and replicate itself using a three step life cycle:
1) It attaches to and enters the host cell using its spike protein.
2) It replicates and synthesizes new proteins and RNA inside the host cell using the cell's machinery. Important viral proteins include PL proteinase, 3CL proteinase and RdRP.
3) The structural and RNA components assemble and are released from the host cell through exocytosis to infect new cells.
Coronaviruses are enveloped viruses with positive-stranded RNA genomes that encode structural and accessory proteins. SARS-CoV-2 enters cells by binding to the ACE2 receptor, and its RNA genome is then translated and replicated to produce more viral proteins and RNA. Assembly and release of new virus particles occurs in the ER and Golgi. The virus can trigger a cytokine storm involving overproduction of IL-6 that may lead to severe immune response and multi-organ dysfunction in some patients.
HCV was discovered in 1989 as a major cause of non-A, non-B hepatitis. It is a single stranded RNA virus of the Flaviviridae family. An estimated 130-170 million people worldwide are chronically infected, making it a significant global health burden.
HCV has an enveloped virion that is 50-80 nm in diameter with E1 and E2 glycoprotein spikes. Its positive-sense single stranded RNA genome is translated into a polyprotein that is cleaved into structural and non-structural proteins. The non-structural proteins NS3, NS4, NS5B are involved in replication and assembly of new virions.
Older treatments for HCV involved peg
Presentation on covide19 and used drug machanismGauriShankar38
SARS-CoV-2 is a betacoronavirus that causes COVID-19. It contains four structural proteins - envelope, spike, membrane, and nucleocapsid. The spike protein binds to the human ACE2 receptor, allowing viral entry. Remdesivir is an antiviral medication used to treat COVID-19. It works by inhibiting the SARS-CoV-2 RNA-dependent RNA polymerase, preventing viral replication. Common side effects include liver and kidney problems. Chloroquine and hydroxychloroquine are also used, and may work by interfering with glycosylation of ACE2 and viral fusion in endosomes.
SARS-CoV-2 and Covid-19: Genetics, Treatment and VaccinesDenish Aloo
The document provides information on SARS-CoV-2 and COVID-19. It discusses the history of past respiratory disease pandemics. It defines coronaviruses and SARS-CoV-2, the virus that causes COVID-19. It describes the taxonomy, structure, genome organization, mutations, and life cycle of SARS-CoV-2. It also discusses the non-structural proteins, structural proteins, and accessory proteins of SARS-CoV-2.
1) SARS-CoV is a coronavirus that emerged in 2002 causing a global pandemic. Its pathogenesis involves aberrant host innate immune responses and viral antagonism of interferon signaling.
2) Models of SARS-CoV infection like human airway epithelial cultures and mouse-adapted SARS-CoV have provided insights into innate immune pathways important for controlling SARS-CoV disease.
3) SARS-CoV encodes several proteins that antagonize type I interferon induction and signaling to evade the host innate immune response, which is an important factor in SARS pathogenesis.
Interferons are glycoproteins that are produced in response to viral infections and other pathogens in order to activate the immune system. There are three main classes of interferons - alpha, beta, and gamma - which signal through different cell surface receptor complexes. Interferons have a variety of antiviral, antitumor, and immunomodulatory properties. They are currently used clinically to treat hepatitis C virus, hepatitis B virus, multiple sclerosis, and some cancers, though their mechanisms of action are still not fully understood. Research on interferons has contributed significantly to the development of molecular biology and our understanding of cytokines.
SARS-CoV-2 has a large RNA genome that it uses to hijack the host cell and replicate itself using a three step life cycle:
1) It attaches to and enters the host cell using its spike protein.
2) It replicates and synthesizes new proteins and RNA inside the host cell using the cell's machinery. Important viral proteins include PL proteinase, 3CL proteinase and RdRP.
3) The structural and RNA components assemble and are released from the host cell through exocytosis to infect new cells.
The document summarizes the HIV lifecycle in cells. It explains that HIV binds to CD4 receptors on cells, fuses with the cell membrane, and injects its RNA inside. The viral enzyme reverse transcriptase then converts the RNA into DNA, which is integrated into the cell's DNA by the integrase enzyme. The cell's machinery then reads the viral DNA and produces viral proteins. These proteins self-assemble into new virus particles that bud out of the cell, taking some cell membrane with them.
This document reports on a study examining how carbon monoxide (CO) induces heme oxygenase-1 (HO-1) expression and inhibits endothelial cell apoptosis triggered by endoplasmic reticulum (ER) stress. The key findings are:
1) CO activates the transcription factor Nrf2 through phosphorylation of the protein kinase R-like ER kinase (PERK), leading to increased HO-1 expression.
2) CO-induced PERK activation results in phosphorylation of eukaryotic translation initiation factor 2α and expression of activating transcription factor 4.
3) CO prevents ER stress-induced expression of X-box binding protein 1 and cleavage of activating transcription factor 6.
4) CO inhibits
Creative Biolabs has extensive experience in coronavirus research. Provide comprehensive high-quality coronavirus (SARS-CoV-2, SARS-CoV, MERS-CoV, etc.) related services and products.
This slide provides a brief introduction to SARS-CoV-2. If you need more knowledge, products and services related to SARS-CoV-2, please follow us.
Agrobacterium detects wounded plant cell phenolics using its VirA/VirG two component sensor system, which induces expression of virulence genes. This allows VirD1 and VirD2 to cut T-DNA from the bacterial plasmid at the right and left borders. VirD2 then attaches to the exposed 5' end of T-DNA, and associates with VIP1 and VIP2 to target the complex to the plant cell nucleus. There, the T-DNA integrates into the plant genome and initiates gall formation.
Immune response in FHM cells following infection with frog virus 3mgray11
This document summarizes a study that examined the differential expression of immune-related genes in fathead minnow cells following infection with frog virus 3 (FV3) or an attenuated 18K knockout mutant. Microarray analysis found that numerous innate and adaptive immune genes were upregulated after wild-type FV3 infection. However, the 18K mutant led to lower expression levels of these genes. This suggests that quantitative differences in gene expression may explain the 18K mutant's attenuated phenotype in vivo. Future studies aim to further analyze host responses to wild-type and mutant viruses to identify key cellular factors involved in protective immunity.
SARS-CoV-2 was first identified in Wuhan, China in late 2019 and has since spread to over 200 countries. It belongs to the coronavirus family and causes the disease COVID-19. The virus enters cells through the ACE2 receptor and replicates its RNA and proteins before being released to infect other cells. Potential treatment strategies include using existing antiviral drugs, developing specific drugs that target the virus genome or proteins, and enhancing immune responses. Ongoing research focuses on antibody development, diagnostic assays, vaccines, and other medical countermeasures to treat and prevent the spread of SARS-CoV-2.
Using SARS-CoV-2 to Teach Physiology and ScienceInsideScientific
Join Dr. Dee Silverthorn for a discussion on how the sudden appearance of the global pandemic of COVID-19 provides a unique opportunity to show students science in action as researchers and healthcare professionals around the world scramble to understand the virus and its effects on the human body. This is the third webinar in this 4-part series on how science education has evolved in the face of new challenges.
In this presentation we will explore some of the ways that we can incorporate today’s headlines into the curriculum by discussing the pathophysiology and pathology of SARS-CoV-2 infection and how it demonstrates the integration of body function across multiple organ systems. Teaching about the coronavirus pandemic also creates opportunities to have students critically analyze research studies and news reports, and to discuss ethical dilemmas such as the distribution of limited amounts of vaccine or the triage of critically ill patients when lifesaving equipment is limited. One important goal of teaching about the coronavirus pandemic is to have students learn to tolerate ambiguity, and to understand that today’s “facts” are simply our best models of what we know.
The document discusses Coronaviruses and COVID-19. It defines Coronaviruses as large, spherical RNA viruses with crown-like spikes that give them their name. COVID-19 is caused by SARS-CoV-2, which binds better than SARS to the ACE2 receptor in humans, causing symptoms ranging from mild to critical illness. The pathogenesis involves viral entry, replication, avoidance of the immune system, and cytokine storm. Diagnosis is via PCR or antigen tests of respiratory or stool samples. Treatment is supportive care, with some antivirals under investigation but none yet approved. Prevention emphasizes social distancing, PPE, sanitization and vaccination research.
This document lists several classes of antiviral drugs including antiherpes agents like acyclovir and famciclovir, antiretroviral agents that target HIV like nucleoside and non-nucleoside reverse transcriptase inhibitors as well as protease inhibitors, and anti-influenza agents amantadine and rimantadine. It then describes the mechanism of action of acyclovir, which involves selective uptake by virus-infected cells, conversion to the active form by a viral enzyme, and inhibition of viral DNA synthesis. Acyclovir is used to treat various herpes virus infections and can cause side effects like nausea, vomiting, and neurotoxicity.
- The mRNA-1273 vaccine induced robust antibody and neutralizing responses against SARS-CoV-2 in all participants after the first dose. A second dose led to even stronger responses, especially in the 100 μg and 250 μg groups. Systemic side effects were mostly mild or moderate. This interim report provides support for mRNA-1273 as a promising COVID-19 vaccine candidate warranting further development and evaluation.
This document analyzes the potential risks of prion disease from Pfizer's COVID-19 mRNA vaccine. It finds that the vaccine's RNA sequence contains elements that could cause the proteins TDP-43 and FUS to take pathological prion confirmations linked to neurodegenerative diseases. Additionally, the vaccine-generated spike protein's interaction with ACE2 may release zinc ions in cells, which are known to facilitate prion formation of TDP-43. The author believes these factors indicate the vaccine was approved prematurely without adequate safety testing and could potentially cause more harm than the disease it is meant to prevent.
Vaccines based on messenger RNA (mRNA) have attracted worldwide attention as Pfizer and Moderna vaccines have been authorized for emergency use by the U.S. Food and Drug Administration (FDA) and similar agencies around the world. This is the first time an mRNA-based vaccine has been approved for use in healthy people, marking an important milestone in the achievements of science and public health.
Chapat et al.-orf1 et orf2 cmi with CIRCOVAC vaccination in sowsMerial EMEA
This study assessed the cell-mediated immune response against PCV2 ORF1 and ORF2 proteins in pigs vaccinated with an inactivated PCV2 vaccine. The results showed that vaccination induced gamma interferon production against both ORF1 and ORF2, primed pigs for interleukin-2 secretion after challenge, and stimulated antibody responses. In contrast, unvaccinated pigs only developed immune responses after challenge. The cellular immune response detected is expected to contribute to reduced PCV2 replication in vaccinated pigs. This highlights the importance of including both ORF1 and ORF2 in PCV2 vaccine design.
1. SARS-CoV-2 infects alveolar epithelial cells expressing ACE2 and RAGE. Cell death releases HMGB1, a ligand of RAGE.
2. HMGB1 binding to RAGE activates signaling pathways like NFkB and increases inflammation. The virus may also mimic HMGB1 to bind RAGE.
3. Soluble RAGE produced from membrane RAGE can bind to Fcgbp and reduce inflammation in the lungs. Genetic variations in RAGE expression impact COVID-19 severity and outcomes like ARDS.
1. SARS-CoV-2 infects alveolar cells expressing ACE2 and RAGE, causing cell death and release of the damage signal HMGB1.
2. HMGB1 binds RAGE and activates signaling pathways increasing inflammation. SARS-CoV-2 may also bind and activate RAGE.
3. Activated RAGE is cleaved to soluble sRAGE which binds ligands and anchors to Fcgbp, reducing inflammation. Insufficient sRAGE or Fcgbp may lead to complications like cytokine storm or death.
This study characterized the function of ALL2, a homolog of ALL1, in the fungal pathogen Cryptococcus neoformans. The key findings were:
1) Unlike deletion of ALL1, deletion of ALL2 attenuated virulence in a pulmonary infection model.
2) The all2Δ mutant shed a less viscous exopolysaccharide and was more sensitive to hydrogen peroxide but more resistant to macrophage killing than the wild type.
3) Transcriptome analysis supported distinct functions for ALL1 and ALL2, with ALL2 uniquely involved in maintaining intracellular pH under low-pH conditions.
This document discusses plant virus induced genes. It explains that after a plant virus enters a host, it can induce genes that lead to either susceptibility or resistance. Susceptible genes provide conditions that allow for a successful viral infection, while resistance genes create antiviral conditions that prevent infection. Virus induced genes can also impact host metabolism and physiology. The document provides examples of susceptible genes involved in viral replication, movement, and suppression of gene silencing defenses.
The document summarizes the HIV lifecycle in cells. It explains that HIV binds to CD4 receptors on cells, fuses with the cell membrane, and injects its RNA inside. The viral enzyme reverse transcriptase then converts the RNA into DNA, which is integrated into the cell's DNA by the integrase enzyme. The cell's machinery then reads the viral DNA and produces viral proteins. These proteins self-assemble into new virus particles that bud out of the cell, taking some cell membrane with them.
This document reports on a study examining how carbon monoxide (CO) induces heme oxygenase-1 (HO-1) expression and inhibits endothelial cell apoptosis triggered by endoplasmic reticulum (ER) stress. The key findings are:
1) CO activates the transcription factor Nrf2 through phosphorylation of the protein kinase R-like ER kinase (PERK), leading to increased HO-1 expression.
2) CO-induced PERK activation results in phosphorylation of eukaryotic translation initiation factor 2α and expression of activating transcription factor 4.
3) CO prevents ER stress-induced expression of X-box binding protein 1 and cleavage of activating transcription factor 6.
4) CO inhibits
Creative Biolabs has extensive experience in coronavirus research. Provide comprehensive high-quality coronavirus (SARS-CoV-2, SARS-CoV, MERS-CoV, etc.) related services and products.
This slide provides a brief introduction to SARS-CoV-2. If you need more knowledge, products and services related to SARS-CoV-2, please follow us.
Agrobacterium detects wounded plant cell phenolics using its VirA/VirG two component sensor system, which induces expression of virulence genes. This allows VirD1 and VirD2 to cut T-DNA from the bacterial plasmid at the right and left borders. VirD2 then attaches to the exposed 5' end of T-DNA, and associates with VIP1 and VIP2 to target the complex to the plant cell nucleus. There, the T-DNA integrates into the plant genome and initiates gall formation.
Immune response in FHM cells following infection with frog virus 3mgray11
This document summarizes a study that examined the differential expression of immune-related genes in fathead minnow cells following infection with frog virus 3 (FV3) or an attenuated 18K knockout mutant. Microarray analysis found that numerous innate and adaptive immune genes were upregulated after wild-type FV3 infection. However, the 18K mutant led to lower expression levels of these genes. This suggests that quantitative differences in gene expression may explain the 18K mutant's attenuated phenotype in vivo. Future studies aim to further analyze host responses to wild-type and mutant viruses to identify key cellular factors involved in protective immunity.
SARS-CoV-2 was first identified in Wuhan, China in late 2019 and has since spread to over 200 countries. It belongs to the coronavirus family and causes the disease COVID-19. The virus enters cells through the ACE2 receptor and replicates its RNA and proteins before being released to infect other cells. Potential treatment strategies include using existing antiviral drugs, developing specific drugs that target the virus genome or proteins, and enhancing immune responses. Ongoing research focuses on antibody development, diagnostic assays, vaccines, and other medical countermeasures to treat and prevent the spread of SARS-CoV-2.
Using SARS-CoV-2 to Teach Physiology and ScienceInsideScientific
Join Dr. Dee Silverthorn for a discussion on how the sudden appearance of the global pandemic of COVID-19 provides a unique opportunity to show students science in action as researchers and healthcare professionals around the world scramble to understand the virus and its effects on the human body. This is the third webinar in this 4-part series on how science education has evolved in the face of new challenges.
In this presentation we will explore some of the ways that we can incorporate today’s headlines into the curriculum by discussing the pathophysiology and pathology of SARS-CoV-2 infection and how it demonstrates the integration of body function across multiple organ systems. Teaching about the coronavirus pandemic also creates opportunities to have students critically analyze research studies and news reports, and to discuss ethical dilemmas such as the distribution of limited amounts of vaccine or the triage of critically ill patients when lifesaving equipment is limited. One important goal of teaching about the coronavirus pandemic is to have students learn to tolerate ambiguity, and to understand that today’s “facts” are simply our best models of what we know.
The document discusses Coronaviruses and COVID-19. It defines Coronaviruses as large, spherical RNA viruses with crown-like spikes that give them their name. COVID-19 is caused by SARS-CoV-2, which binds better than SARS to the ACE2 receptor in humans, causing symptoms ranging from mild to critical illness. The pathogenesis involves viral entry, replication, avoidance of the immune system, and cytokine storm. Diagnosis is via PCR or antigen tests of respiratory or stool samples. Treatment is supportive care, with some antivirals under investigation but none yet approved. Prevention emphasizes social distancing, PPE, sanitization and vaccination research.
This document lists several classes of antiviral drugs including antiherpes agents like acyclovir and famciclovir, antiretroviral agents that target HIV like nucleoside and non-nucleoside reverse transcriptase inhibitors as well as protease inhibitors, and anti-influenza agents amantadine and rimantadine. It then describes the mechanism of action of acyclovir, which involves selective uptake by virus-infected cells, conversion to the active form by a viral enzyme, and inhibition of viral DNA synthesis. Acyclovir is used to treat various herpes virus infections and can cause side effects like nausea, vomiting, and neurotoxicity.
- The mRNA-1273 vaccine induced robust antibody and neutralizing responses against SARS-CoV-2 in all participants after the first dose. A second dose led to even stronger responses, especially in the 100 μg and 250 μg groups. Systemic side effects were mostly mild or moderate. This interim report provides support for mRNA-1273 as a promising COVID-19 vaccine candidate warranting further development and evaluation.
This document analyzes the potential risks of prion disease from Pfizer's COVID-19 mRNA vaccine. It finds that the vaccine's RNA sequence contains elements that could cause the proteins TDP-43 and FUS to take pathological prion confirmations linked to neurodegenerative diseases. Additionally, the vaccine-generated spike protein's interaction with ACE2 may release zinc ions in cells, which are known to facilitate prion formation of TDP-43. The author believes these factors indicate the vaccine was approved prematurely without adequate safety testing and could potentially cause more harm than the disease it is meant to prevent.
Vaccines based on messenger RNA (mRNA) have attracted worldwide attention as Pfizer and Moderna vaccines have been authorized for emergency use by the U.S. Food and Drug Administration (FDA) and similar agencies around the world. This is the first time an mRNA-based vaccine has been approved for use in healthy people, marking an important milestone in the achievements of science and public health.
Chapat et al.-orf1 et orf2 cmi with CIRCOVAC vaccination in sowsMerial EMEA
This study assessed the cell-mediated immune response against PCV2 ORF1 and ORF2 proteins in pigs vaccinated with an inactivated PCV2 vaccine. The results showed that vaccination induced gamma interferon production against both ORF1 and ORF2, primed pigs for interleukin-2 secretion after challenge, and stimulated antibody responses. In contrast, unvaccinated pigs only developed immune responses after challenge. The cellular immune response detected is expected to contribute to reduced PCV2 replication in vaccinated pigs. This highlights the importance of including both ORF1 and ORF2 in PCV2 vaccine design.
1. SARS-CoV-2 infects alveolar epithelial cells expressing ACE2 and RAGE. Cell death releases HMGB1, a ligand of RAGE.
2. HMGB1 binding to RAGE activates signaling pathways like NFkB and increases inflammation. The virus may also mimic HMGB1 to bind RAGE.
3. Soluble RAGE produced from membrane RAGE can bind to Fcgbp and reduce inflammation in the lungs. Genetic variations in RAGE expression impact COVID-19 severity and outcomes like ARDS.
1. SARS-CoV-2 infects alveolar cells expressing ACE2 and RAGE, causing cell death and release of the damage signal HMGB1.
2. HMGB1 binds RAGE and activates signaling pathways increasing inflammation. SARS-CoV-2 may also bind and activate RAGE.
3. Activated RAGE is cleaved to soluble sRAGE which binds ligands and anchors to Fcgbp, reducing inflammation. Insufficient sRAGE or Fcgbp may lead to complications like cytokine storm or death.
This study characterized the function of ALL2, a homolog of ALL1, in the fungal pathogen Cryptococcus neoformans. The key findings were:
1) Unlike deletion of ALL1, deletion of ALL2 attenuated virulence in a pulmonary infection model.
2) The all2Δ mutant shed a less viscous exopolysaccharide and was more sensitive to hydrogen peroxide but more resistant to macrophage killing than the wild type.
3) Transcriptome analysis supported distinct functions for ALL1 and ALL2, with ALL2 uniquely involved in maintaining intracellular pH under low-pH conditions.
This document discusses plant virus induced genes. It explains that after a plant virus enters a host, it can induce genes that lead to either susceptibility or resistance. Susceptible genes provide conditions that allow for a successful viral infection, while resistance genes create antiviral conditions that prevent infection. Virus induced genes can also impact host metabolism and physiology. The document provides examples of susceptible genes involved in viral replication, movement, and suppression of gene silencing defenses.
ANTI-VIRAL HERBAL PHYTOCONSTITUENTS OF TULSI (OCIMUM SANCTUM) AGAINST COVID-1...Yamini Shah
This document discusses potential herbal treatments for COVID-19 from Tulsi plant extracts. It summarizes the rationale, objectives, and introduction to SARS viruses. Molecular docking studies show good binding affinity of chicoric acid, rosmarinic acid, and caftaric acid from Tulsi with SARS-CoV-2 proteins. Formulations for herbal mouthwash, gargle, nasal spray, nasal gel and throat paint were developed using Tulsi and evaluated for stability and efficacy.
Antisense RNA is the complementary RNA to the protein-coding messenger mRNA. The antisense mRNA binds to sense mRNA and the translation was restricted, that is called translation arrest. The nature antisense RNA technology present in hok &sok in E.coli R1 plasmid. The artificial or purpose antisense RNA technology best example is flavr savr tomato.
Chlorogenic acid may be a potent inhibitor of dimeric SARS-CoV-2 main proteas...LucyPi1
Abstract Background: Since the emergence of coronavirus disease 2019 to date, there is no available approved drug or definitive treatment for coronavirus disease 2019 viral infection, and the identification of novel hits against therapeutic targets has become a global emergency. Echinacea purpurea is a traditional herb utilized to treat cough, fever, sore throat, respiratory tract infection, and so on as an immune stimulant. In this study, in silico molecular docking approach was used to screen phytocompounds from E. purpurea against severe acute respiratory syndrome coronavirus 2 main protease 3C-like protease (3CLpro) and severe acute respiratory syndrome coronavirus main peptidase (96% sequence similarity) to blunt the viral gene expression and viral replication. Methods: Initially, we screened phytocompounds for their druggability and ADMET property. Furthermore, x-ray crystallographic structures of main proteases 3CLpro and main peptidase having Protein Data Bank ID 6LU7 and 2GTB were used as protein targets for the identification of potential drug candidates. We performed docking using AutoDock Vina by PyRx 0.8 software. BIOVIA Discovery Studio Visualizer v2019 was used to analyze ligand-protein complex. The probable protein targets of the selected compound were predicted by BindingDB (P ≥ 0.7). STRING and Kyoto Encyclopedia of Genes and Genomes pathways are utilized to identify the molecular pathways modulated by the predicted targets (FDR ≤ 0.05), and the network interaction between compounds and protein pathways was constricted by Cytoscape 3.6.1. Results: Among all the compounds, chlorogenic acid showed druggable characteristics and scored the lowest binding energy with main protease and main peptidase via interacting with active site 1 domain amino acid residues. Interestingly, chlorogenic acid interacted with Phe140 main protease 3CLpro, which is potentially involved in the dimerization. Enrichment analysis identified chlorogenic acid to modulate insulin resistance, necroptosis, interleukin-17, tumor necrosis factor signaling pathway, legionellosis, T helper 17 cell differentiation, advanced glycation end products and receptor for advanced glycation end products, mitogen-activated protein kinase, Ras, estrogen, vascular endothelial growth factor, B-cell receptor, nuclear factor kappa B, Rap1, hypoxia inducible factor-1, phosphatidylinositide 3-kinase-Akt, insulin, mechanistic target of rapamycin, p53, retinoic acid inducible gene I like receptor, and ErbB signaling pathways. Conclusion: Chlorogenic acid may act as a potent main protease 3CLpro inhibitor and may also inhibit the severe acute respiratory syndrome coronavirus 2 dimerization, viral gene expression, and replication within the lung epithelium. Chlorogenic acid may go a long way in finding one of the multipronged solutions to tackle coronavirus disease 2019 viral infection in the future.
The entry mechanism of corona virus into the host cell.SayanKar9
The document summarizes the entry, replication cycle, and transmission of coronavirus in host cells. It discusses that coronavirus binds to ACE2 receptors on host cells and enters via endosomes. The viral RNA is released and replicates, producing more RNA and structural proteins. New virions are assembled and released from the host cell through vesicles and exocytosis. Coronavirus utilizes its RNA polymerase and produces subgenomic mRNA to hijack the host cell's machinery and replicate efficiently. The replicated virions then infect other cells, completing the coronavirus life cycle.
This document provides information on the phenotype and genotype of COVID-19. It discusses that coronaviruses are RNA viruses that cause respiratory infections in humans. COVID-19 is caused by a novel betacoronavirus. The virus particle is spherical with spikes and enters cells by binding to the ACE2 receptor. It contains a positive-sense RNA genome that is translated and replicated via a replicase-transcriptase complex to make structural proteins and more virus particles.
- SARS-CoV-2 is a novel coronavirus that causes COVID-19 and primarily spreads through respiratory droplets. It attaches to human cells through ACE2 receptors and CD147 receptors.
- Certain ACE2 receptor polymorphisms may increase or decrease susceptibility to SARS-CoV-2 infection. A recombinant soluble ACE2 protein is in clinical trials to treat COVID-19.
- A CD147 antibody called meplazumab may effectively inhibit SARS-CoV-2 infection and cytokine storm, even against variants like Delta. Meplazumab works by blocking viral entry through ACE2 and CD147 receptors.
A detailed description of HIV covering virology, morphology, pathogenesis, clinical stages and manifestations, laboratory diagnosis, and diagnostic strategy, and therapeutic options and prevention.
a) Describe two ways the researcher could minimise experimenter bias i.docxbickerstaffinell
a) Describe two ways the researcher could minimise experimenter bias in this study.
b) Describe a way the researchers could minimise sample bias in this study. (distinct from your answers in part a)
Nuclear import of SARS-CoV-2 nucleocapsid (N) protein is not inhibited by overmectin B.A. Loney* and M.A. Larkey* *Bundoora Institute for Applied Medical Research. Introduction The causative agent of the current COVID-19 pandemic, SARS-CoV-2, is a single stranded positive sense RNA virus that is closely related to severe acute respiratory syndrome coronavirus (SARS-CoV). It has been previously shown that SARS-CoV-2 nucleocapsid (N) is present in the cytoplasm but can also actively localize to the nucleolus where it can interact with host proteins and also bind to viral RNA. It has also been previously shown that nuclear import of similar nucleocapsid proteins (including the HIV-1 nucleocapsid protein, NC) from other RNA viruses can be inhibited by the drug overmectin resulting in decreased viral replication efficiency. There are multiple nuclear import pathways mediated by different receptors. The two most common nuclear import pathways are mediated by the importin / heterodimer or by the importin homodimer. Overmectin has previously been demonstrated to inhibit nuclear import by disrupting the importin / pathway. In this study SARS-CoV-2 nucleocapsid (N) was transfected into Hela cells and the effectiveness of overmectin at inhibiting its nuclear import was determined. Methods Expression of N protein in the absence of other viral proteins. To investigate the nuclear import of SARS-CoV-2 N protein three constructs were created. 1. pEGFP-NCov2. The N gene (from SARS-CoV-2, isolate BJ04) was cloned into the eukaryotic expression vector pEGFP-C1 (Promega) such that expression of the N gene was under the control of a cytomegalovirus (CMV) polymerase Il promoter to express an N protein fusion with the C-terminal of EGFP. 2. pEGFP. The pEGFP-C1 expression vector alone. 3. EEGFP-TRF1. A positive control for nuclear import. The human TRF1 gene was cloned into the eukaryotic expression vector pEGFP-C1 to express an N protein fusion with the C-terminal of EGFP. TRF1 nuclear localisation has shown to be mediated by the importin homodimer. Hela cells were cultured in 12 separate culture plates at a density of 1 0 5 cells per 9.6 cm 2 plate with each plate containing 2 coverslips. Cells were cultured using Cell Biologics' Culture Complete Growth Medium with 5\% foetal calf serum at 3 7 C and 5% CO 2 . Cells were transfected with 2 g of either pEGFPNCov2 (plates 1,4,7 and 10), pEGFP (plates 2, 5, 8 and 11) or pEGFP-TRF1 (3, 6, 9 and 12) and 50 g of Lipofectamine (GibcoBRL). 12 hours post-transfection, even numbered plates were treated with 5 M overmectin in DMSO and odd numbered plates were left untreated. After 24 hours coverslips were removed, and the cells fixed. DAPI was added to visualise the nuclei and the localisation of GFP determined by fluorescent mic.
This document discusses recent advances in the study of hemoparasites like Plasmodium, Babesia, Leishmania, and Trypanosoma. It covers new understandings in pathogenesis, improved diagnostic techniques like PCR and rapid tests, and novel treatment approaches including artemisinin derivatives and vaccines. Key areas covered include identifying parasite proteins involved in host invasion, endothelial receptors in malaria sequestration, diagnostic targets such as HRP-2 and pLDH, combination therapies for drug resistance, and vaccine candidates targeting different parasite stages.
This document discusses antiviral drugs and summarizes their mechanisms and classifications. It describes how viruses work at a cellular level and replicates inside host cells. It then classifies antiviral drugs based on their mechanism of action, including how they target different stages of the viral life cycle like entry, replication, assembly and release. Specific drugs are explained like amantadine, which targets influenza viruses, and nucleoside analogues including acyclovir which act as chain terminators during viral DNA synthesis. Interferons are also summarized as potent natural antiviral proteins produced by infected cells.
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2. TANGY, SOUR AND SWEET, ALL AT THE
SAME TIME, THE POMEGRANATE IS THE
TRUE HARBINGER OF THE AUTUMN
Pomegranate has been used for thousands of years to cure a wide range of
diseases across different cultures and civilizations
In indigenous medicine pomegranate is considered ‘a pharmacy unto itself’
It was lauded in ancient times in the old testament of bible, the Jewish
Torah, and the Babylonian Talmud as a sacred fruit confirming power of
fertility, abundance and good luck.
2
3. 3
Phytochemicals of pomegranates can be successfully used in controlling the various types of
carcinomas out of which some share the same biological pathways as that of SARS COV-2
ARDS is the leading course of the death in SARS COV-2 infection which is associated with the
upregulation of proinflammatory cytokines expression which is called cytokine storm.
Pomegranate juice and peel extracts contained 124 different types of antioxidants and
bioactive substance like polyphenols which can attenuate SARS COV-2 and its clinical outcome.
6. COVID 19 INFECTION
Caused by SARS COV-2 virus
Newly emerge SARS COV-2 pandemic affected more than ten million world population
Most of the fatalities was due to multi organ failure following acute respiratory distress syndrome (ARDS).
There were several endemics due to corona virus in the recent history
1) Severe acute respiratory distress syndrome corona virus SARS COV
2) Middle east respiratory syndrome corona virus MERS-COV
Source of origin and exact pathogenicity SARS COV-2 is not fully understood up to the date.
6
7. SARS COV-2 - beta corona virus
80% mild illness
14% lung involvement with dyspnea and hypoxia.
5% develop ARDS, shock and multi organ dysfunction.
Average death rate - 2.3% , can vary from 01 to 9 %.
It has four structural proteins which are similar to other corona viruses. Spike (s), Envelop(e),
Membrane(m) and Nucleocapsid(n) proteins
7
COVID 19… Continued
9. 9
Spike proteins are cleavage into S1 and S2 subunits by host cell proteases
S1 contained receptor binding domain for antigen converting enzyme 2(ACE2) to bind with host cell
leading to viral infection
In SARS COV-2 spike proteins is cleavage into S1 and S2 subunits by the host cell protease, most
evidently by TMPRSS2 (Trance Membrane Protein Serine S2)
Less evidently by Cathepsin and Furin
STRUCTURE OF SARS COV-2
10. POSSIBLE
CLEAVAGE
MECHANISMS
(A) STRUCTURES OF THREE COMMON HOST CELL
PROTEASES KNOWN TO ACTIVATE
CORONAVIRUS TRYPSIN , FURIN AND
CATHEPSIN L
(B) DIAGRAM OF A CORONAVIRUS LIFE CYCLE AND
THE VARIOUS HOST CELL PROTEASES KNOWN
TO CLEAVE AND ACTIVATE SOME
CORONAVIRUS S PROTEINS. INHIBITORS OF
HOST CELL PROTEASES, INCLUDING TMPRSS2,
CATHEPSINS AND FURIN, HAVE BEEN
PROPOSED AS POTENTIAL ANTIVIRAL
THERAPEUTICS FOR CORONAVIRUS
INFECTIONS
A
B
10
11. MAIN PATHOPHYSIOLOGICAL SEQUENCES OF SARS
COV-19 INFECTION
1. Rapid viral replication
2. Cytokine storm
3. Immune dysfunction
4. Oxidative stress and
5. Delayed apoptosis
Pomegranate fruit extract may be effective in each and every step of SARS COV-2 infection and its
clinical outcome.
11
12. ELLAGITANNIN OF POMEGRANATE CAN
INHIBIT THE TMPRSS2
TMPRSS2 is essential for viral entry in to host cells. (This gene expression is up regulated in androgen
dependent prostatic cancers)
Ellagitannin of pomegranate can inhibit the TMPRSS2.
Pomegranate juice obtained by squeezing the whole fruit has the highest concentration of
ellagitannins than any commonly consumed juice.
Pomegranate extract rich in ellagitannin inhibits the viral entry.
12
13. Furin is a serine protease which is also suggested to mediates the cleavage of the spike protein
in to S1 and S2 sub units during viral entry
SARS COV-2 spike protein harbors a Furin cleavage site at S1/S2 boundary which is not available
in other corona viruses.
Furin is abundant in respiratory tract. SARS COV-2 may successfully exploit Furin to activate
surface glycoproteins to its pathogenicity.
Quercetin and epigallocatechin gallate (EGCC) which are found in pomegranate can inhibit
Furin and thereby inhibit the viral entry in to the host cells.
QUERCETIN AND EPIGALLOCATECHIN GALLATE
(EGCC) INHIBITS FURIN
13
14. CATHEPSINS Found in endosomes and lysosomes and function as degradative enzymes
Cathepsin selectively cleave protein by cutting the peptide bonds that links specific amino acids
It may mediate the membrane fusion function and cleavage of the spike proteins
Pomegranate peel extract shows strong inhibitory effect on cathepsin activity. Cathepsin
inhibitory properties of pomegranate fruit extract may be a potential mechanism which can be
utilize to prevent viral entry in to the host cell
POMEGRANATE PEEL EXTRACT SHOWS STRONG
INHIBITORY EFFECT ON CATHEPSIN
14
15. POMEGRANATE INHIBITS ALL 03 POSSIBLE
CLEAVAGE MECHANISMS OF SARS COV-2
15
TMPRSS2
FURIN
CATHEPSIN
16. VIRAL ENTRY
Is mediated by binding of the spike (s) protein with cell surface angiotensin converting enzyme
2 (ACE2) receptors
ACE2 can be found in lungs, heart, kidneys and intestine
The highest density of ACE2 can be found in type 2 pneumocyte of alveoli
SARS COV-2 shows twenty times more affinity to ACE2 than SARS virus
After entering genomic RNA (RNA+) release in to host cell cytoplasm. The genomic RNA is used
to make RNA dependent RNA polymerase which regulate the production of new genomic RNA’s
16
18. ZINK BLOCK THE RNA DEPENDENT RNA
POLYMERASE
RNA Dependent RNA Polymerase (RDRP) of sars-cov-2 is essential for viral replication
Zink block the RDRP.
• Pomegranate is the second-best source of zinc behind the avocado
• Quercetin and Epigallocatechin-gallate of pomegranate fruit extract function as a zinc
ionophores to facilitate transportation of zinc across the cell membrane.
• Therefor consumption of pomegranate may reduce the viral replication.
18
19. POMEGRANATE EXTRACT DOWN REGULATES
THE VALOSIN CONTAINING PROTEIN (VCP)
EXPRESSION
VCP Is belongs to ATPase super family. Genome-wide screen reveals VCP requirement for
coronavirus exit from endosomes. Inhibition of a VCP resulted in virus accumulation in early
endosome
Pomegranate extract down regulates the VCP expression and thereby reduce the virus release
from endosome. Decrease in expression of VCP also reduces the effects of NF-kB induced
inflammatory cascade
20
20. LUTEOLIN AND KAEMPFEROL INDUCE
APOPTOSIS
Delayed apoptosis
Apoptosis is a host defense mechanism against viral replication and proliferation.
Vires can inhibit apoptotic pathway, thereby prolong the survival of virus inside the host cells
to maximize the production of virus progeny
21
21. LUTEOLIN AND KAEMPFEROL INDUCE
APOPTOSIS
Luteolin and Kaempferol can be found in the pomegranate. Both substances can induce
apoptosis via several mechanisms
Increase intracellular Reactive oxygen species (ROS) levels and induce apoptosis
Decrease the Bcl2/Bax ratio in viral infected cells promote cell death
Trigger activation of p53
(The p53 transcription factor prevents tumor development through induction of cell cycle arrest
and cell death by apoptosis. As many as several hundreds of genes or more are regulated by
p53. Some virus delays the apoptosis by inhibition of p53. Kaempferol and Luteolin trigger
activation of p53)
22
23. DELPHINIDIN INHIBITS INTERGRINS/PI-
3K/MAPK
INTEGRINS Are heterogenic cell surface receptors. They are involved in cells adhesion, migration,
signaling, and angiogenesis.
Binding spike protein with integrin heteromers activate transduction pathways involving
phosphatidylinositol-3-kinase (pi-3k) or Mitogen Activator Protein Kinase (MAPK) which promote the
viral entry
Rgd motif of the spike protein of the SARS COV-2 shows a strong affinity to integrins, particularly
𝛼𝑣𝛽3. Rgd motif is absent in all other corona viruses. It is believed integrins may work as alternative
receptor for SARS COV-2 entry
Delphinidin of pomegranate extract has proven to be effective in inhibition of intergrins, pi-3k and
MAPK expression. Therefore, delphinidin is a potential molecule which can prevent SARS COV-2
entry in to host cell by blockage of above-mentioned mechanism.
24
24. PUNICALAGIN OF POMEGRANATE RESTORE NK CELL
FUNCTIONS
• Total number of NK cells and Their functions are markedly depleted COVID-19 infection.
• Functions of the NK cells are exhausted with the increased expression of NKG2A.
• NKG2A is a ligand which binds to inhibitory NK cells receptor (iNKR’s) and suppress the NK cells.
PUNICALAGIN OF POMEGRANATE JUICE DOWN REGULATE EXPRESSION OF NKG2A
25. 26
HOW POLYPHENOL'S OF POMEGRANATE
INVOLVE IN ATTENUATION OF
INFLAMMATION AND PREVENT ARDS IN SARS
COV-2
26. SARS COV-2 DOWN REGULATE ACE2 AND
UPREGULATE ACE1
27
SARS COV-2 spike protein binds to the. ACE2
which is a natural protector against lung injury.
With the viral infection ACE2 is down regulated
and in compensation ACE 1 is up regulated.
Excess amount of angiotensin 2 production via
ACE1
Uncontrolled angiotensin 2 cause over
stimulation of type 1a angiotensin receptors
(AGTR 1a) leading to increase vascular
permeability in the lungs witch leads to ARDS.
27. CYTOKINE STORM
ARDS is associated with up regulation of pro inflammatory cytokines production called ‘cytokine
storm’
Interleukin 1𝛽. Il-1, il-6, il-8, cc chemokine ligand 2 (ccl-2), cxc chemokine ligand 10 (cxcl-10),
interferon 𝛼(anti-viral substance release from the infected cells), interferon−𝛾 (anti-viral
substance release from the immune cells)’
Initial onset of rapid viral replication causes massive epithelial and endothelial damage are
those which associate with hypercytokinemia and increase mononuclear macrophages and
neutrophil infiltration
28
28. THE MAJOR ANTHOCYANINS OF
POMEGRANATE INHIBIT NUCLEAR FACTOR
KAPPA BETA (NF-kB)
• Nuclear factor kappa beta (NF-kB) is a transcription protein complex.
• NF-κB pathway involves viral replication, delaying apoptosis and
modulating host immune response which leads to increase production
of IL-2, IL-6, IL-8, TNF-𝛼
Delphinidin, Cyanidin, Pelargonidin, the major anthocyanins of
pomegranate juice show potent inhibitory effects on NF-kB
ARDS
29. MAJOR ANTHOCYANINS OF THE POMEGRANATE
INHIBITS VASCULAR ENDOTHELIAL GROWTH
FACTOR (VEGF)
Vascular Endothelial Growth Factor (VEGF) pays a pivotal role in
both angiogenesis and microvascular permeability in ARDS acute
lung injury (ALI)
Major anthocyanins of the pomegranate peel have shown to
suppress VEGF via following pathways.
Delphinidin inhibit TNF𝛼 induced VEGF receptor expression in
endothelial cells whereas ellagitannin inhibit VEGF via PIK/akt
pathway.
30
30. DELPHINIDIN VS FIBROBLAST GROWTH FACTORS (FGF)
• Fibroblast growth factors (FGF) directly corelate with morbidity and mortality in ARDS.
Delphinidin of pomegranate peel extract has proven its regulatory potentials in pathological
conditions associated with over expression of FGF in number of clinical studies.
32. ANTHOCYANINS OF POMEGRANATE
STIMULATE TISSUE INHIBITORS OF MMPS
(TIMP-2)
Matrix metalloproteinases (MMPS) involved in degradation of extracellular matrix.
These molecules can act independently and in coordinate manner via activation of tyrosine
regulatory pathway in development of ARDS
Anthocyanins of pomegranate stimulate tissue inhibitors of MMPS (TIMP-2) and Plasminogen
Activator Inhibitor (PAI) both of which counteract MMPS and Urokinase Plasminogen Activator UPA
33
33. P38 Mitogen-activated protein kinase (p38 MAPK) belongs to the map kinase superfamily.
Activation of p38 MAPK has been reportecells infected with SARS-COV
p38 MAPK inhibitors can suppress Il-6 and TNF-𝛼 expression in monocytes and mast cells.
p38 MAPK signaling pathway supposed to be one of the main mechanisms of acute lung
injury and ARDS
DELPHINIDIN OF POMEGRANATE EXTRACT INHIBITS p38 MAPK PATHWAY
DELPHINIDIN OF POMEGRANATE INHIBITS P38
MAPK SIGNALIN PATHWAY
34
35. FLAVONOIDS OF POMEGRANATE REDUCE THE
OXIDATIVE STRESS
Free radicals can attract inflammatory mediators which contribute to the inflammatory response
and tissue damage in ARDS.
• Flavonoids can interfere with different free radical forming pathways.
1. direct radical scavenging
2. nitric oxide pathway
3. xanthene oxidase pathway
It has been shown when pomegranate whole fruit extract given to the patient with acute
inflammation, it causes reduction of serum Malonaldehyde levels which is a biological marker of
oxidative stress in cell membrane injury
36.
37. ANTHOCYANINS INHIBITS ICAM-1 AND
VCAM-1
• Upon cytokine stimulation, ICAM-1 (intra cellular adhesion molecule) and VCAM-1 (vascular cell
adhesion molecule) expression significantly upregulated in ARDS.
• ICAM‐1, and VCAM‐1 are implicated in the interactions between leukocytes and the
endothelium during the inflammatory process what is called the “adhesion cascade”.
Delphinidin, Cyanidin, Pelargonidin and their metabolites have shown strong inhibitory effects on
ICAM-1 and VCAM-1.
Gallic acid which is abundant in pomegranate peel, decrease the expression of ICAM-1 and VCAM-
1
38. OTHER MECHANISMS WHICH INVOLVE IN
ATTENUATION OF INFLAMMATION AND PREVENT
ARDS IN SARS COV-2
• COX-2 is the enzyme largely responsible for causing inflammation. Delphinidin inhibits TNF α induce
expression of COX-2.
• Delphinidin directly bind with Fyn kinase and inhibit its function. Fyn kinase
inhibitors has shown to be effective treatment in SARS.
• Punicalagin attenuate the lipopolysaccharide (LPS) induce release of NO, TNF 𝛼 and
IL6 in the setting of acute inflammation.
• Heme oxygenase 1(HO-1) activation through pi3k/akt pathway plays critical role in
protection of lungs in oxidative injury in the setting of sepsis. punicalagin shows
antioxidant activity via increasing N𝛾F2 mediated HO-1 expression and pi3k/akt
mediated HO-1 expression.
39. CONCLUSION
Rapid viral replication, cytokine storm, immune dysfunction, oxidative stress, delayed apoptosis are
the main pathophysiological sequences of SARS COV-19 infection
In conclusion this study provides new insight about the mechanisms by which varies types of
polyphenols of pomegranate extract works against SARS COV-2 infection and viral induce inflammatory
reaction
We suggest further study preferably in vivo is necessary to determine whether or to what extent,
the polyphenols of pomegranate and their metabolites play roles in prevention and management of
SARS COVID 19 infection.
With the back ground of tremendous impact of SARS COV-2 infection on global health and with the
paucity or lack of therapeutic measures, it is worth trying pomegranate juice and peel extract as a
prophylactic, anti-viral and anti-inflammatory agent based on the available knowledge as it has been
used in several systems of medicine since antient time without significant side effects. 40
41. EAT POMEGRA DAY
KEEP COVID AWAY
POMEG IN THE MORNING
DR. DINESH’S WARNING //
POMEG AT NIGHT
KILL THE COVID OUT RIGHT
POMEG WITH BLENDED PEEL
COVID WILL INSTANT HEAL
EAT EACH DAY SEVEN DAYS A WEEK
READY ALL READY TO HEAL
42. THANK YOU!
43
Dr.Dinesh Amarasekara
Department of Urology
Sri Lanka National Hospital, Colombo.
E mail. ddnanditha@gmail.com
ddnanditha@yahoo.com
Phone No. +94716890949
Address. 420/32, ‘Sanketha’,
Walipara,Thalawathugoda,Colombo
Sri Lanka.
Zip Coad 10116
Editor's Notes
IT HAS YET TO BE PROVEN WHETHER, AND AT WHICH POSITION, CATHEPSIN L PARTICIPATE IN PATHOGENESIS OF NOVEL SARS COV-2 INFECTION
REPLICATION FIRST PRODUCE ANTI-SENSE RNA (RNA_) WHICH IS TRANSCRIBE IN TO SEVERAL SUB GENOMIC M-RNA’S BY DISCONTINUES TRANSCRIPTION. THIS SUB GENOMIC M-RNA’S TRANSLATE IN TO SEVERAL STRUCTURAL PROTEINS E.G. NAP-3, NSP-4, NSP-6, SPIKE, ENVELOPE, MEMBRANE PROTEIN. RNA_ REPLICATE IN TO GENOMIC RNA(RNA+) AND COMBINED WITH VIRAL PROTEINS TO FORM A VIRION PROGENY
THE NONSTRUCTURAL PROTEINS ANCHOR THE NOVEL VIRUS IN TO THE ENDOPLASMIC RETICULUM TO FORM A DOUBLE MEMBRANE VESICLE. ENDOPLASMIC RETICULUM GOLGI INTERMEDIATE COMPARTMENT (ERGIC) VIA SECRETORY PATHWAY MAKE A VIRUS PROGENY WHICH IS EXPEL FROM THE CELL BY EXOCYTOSIS
RDB motif (peptide sequence with arginine, glycine, aspartic acid) of the spike protein . (N.B. INTEGRIN BINDING MAY BE A PROMISING THERAPEUTICS TARGET, AND SHOULD BE TESTED EXPERIMENTALLY
Therefor punicalagin of pomegranate would be a good agent to overcome the SARS COV-2 resistant to NK-cells