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Current Epidemiological and Clinical Features of COVID-19; a Global Perspective From China
Published in William C. Cockerham, Geoffrey B. Cockerham, The COVID-19 Reader, 2020
Huilan Tu, Sheng Tu, Shiqi Gao, Anwen Shao, Jifang Sheng
SARS-CoV-2 was found to be a positive-sense, single-stranded RNA virus belonging to the Betacoronavirus B lineage and is closely related to the SARS-CoV virus.13 Full-length genome sequences were obtained and indicated that the SARS-CoV-2 genome shares 79.6% sequence identity with that of SARS-CoV.14 Notably, SARS-CoV-2 infects human lung alveolar epithelial cells through receptor-mediated endocytosis using angiotensin-converting enzyme II (ACE2) as an entry receptor. Attachment to the receptor mediates the subsequent fusion between the viral envelope and host cell membrane, thereby allowing viral entry into the host cell.15,16
Targeting Gene Expression to the Lung
Published in Kenneth L. Brigham, Gene Therapy for Diseases of the Lung, 2020
Jeffrey A. Whitsett, Stephan W. Glasser
A wide variety of vectors are being developed for gene transfer including viruses, liposomes, and protein-DNA conjugates. Recombinant viral vectors, including adenoviruses, retroviruses, and adeno-associated viruses, enter target cells based on presence of viral proteins that interact with cell surfaces. The efficiency of viral entry is often highly species and cell type-specific—e.g., ecotropic and amphotropic retroviruses, which bind to distinct cell transport proteins on the surface of the cell. The abundance or absence of specific cell surface receptors may strongly influence the ability of a viral vector to transfect the target cell and, in turn, may be influenced by cell differentiation and proliferation that alters the efficiency of viral entry and transport of DNA to the nucleus.
Chikungunya virus and Japanese encephalitis virus
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
The surface glycoproteins E1 and E2 form a heterodimer and mediate cell entry. E2 is principally involved in attachment, at which point E1 becomes involved in membrane fusion. Viral entry into the cell then occurs by endocytosis. Viral replication occurs in the cell cytosol. The structural proteins are involved in encapsidation and budding, with a layer of host membrane enveloping the virus for release. This process is similar for all alphaviruses [1].
Design and statistical optimisation of emulsomal nanoparticles for improved anti-SARS-CoV-2 activity of N-(5-nitrothiazol-2-yl)-carboxamido candidates: in vitro and in silico studies
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Ahmed A. Al-Karmalawy, Dalia S. El-Gamil, Rabeh El-Shesheny, Marwa Sharaky, Radwan Alnajjar, Omnia Kutkat, Yassmin Moatasim, Mohamed Elagawany, Sara T. Al-Rashood, Faizah A. Binjubair, Wagdy M. Eldehna, Ayman M. Noreddin, Mohamed Y. Zakaria
The possible mode of action for the most potent EMLs formula (F3e) towards SARS-CoV-2 inhibition was examined at three different stages of the virus propagation cycle and based on three main possible modes of action:The direct effect of each extract is to inactivate the virus viability (virucidal activity).The ability of each extract to inhibit the attachment of the virus to infected cells – membrane fusion is known to block the viral entry (viral adsorption).Inhibition of budding and viral replication.
Zinc pyrithione is a potent inhibitor of PLPro and cathepsin L enzymes with ex vivo inhibition of SARS-CoV-2 entry and replication
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2022
Jerneja Kladnik, Ana Dolinar, Jakob Kljun, David Perea, Judith Grau-Expósito, Meritxell Genescà, Marko Novinec, Maria J. Buzon, Iztok Turel
The viral entry assay was used to determine how effective the compounds tested (a, 1a, 2a) were in preventing the entry of pseudoviral particles carrying the SARS-CoV-2 S protein into HLT cells at concentrations of 30 µM, 10 µM, 1 µM, and 0.5 µM (Figure 3(a)). Viral entry was inhibited in a concentration-dependent manner. At 30 µM, zinc and ruthenium complexes, 1a and 2a, respectively, had comparable effects with an inhibition of 93.12% and 93.16%, respectively, while ligand a showed an inhibition of 86.41%. The observed difference in inhibition between the complexes is more pronounced at 10 µM, where zinc complex 1a inhibited viral penetration by 91.18%, ruthenium complex 2a by 83.9% and ligand a by 74.34%. When ligand a was tested at 1 µM and 0.5 µM, it inhibited viral entry by 16.67% and 15.33%, respectively, while ruthenium complex 2a showed an inhibition of 36.7% and 34.54%, respectively, and zinc complex 1a showed 51.80% and 40.44% inhibition at the same concentrations. Thus, calculated IC50 values were 0.84 µM for 1a, 4.66 µM for 2a, and 5.19 µM for a. Similar to enzyme inhibition assays, ligand a was therefore found to be the worst inhibitor of viral entry, followed by ruthenium complex 2a and zinc complex 1a. Moreover, zinc also contributes to better inhibition of viral entry than ruthenium.
Diagnosis, prevention, and treatment of coronavirus disease: a review
Published in Expert Review of Anti-infective Therapy, 2022
Manoj Kumar Sarangi, Sasmita Padhi, Shrivardhan Dheeman, Santosh Kumar Karn, L. D. Patel, Dong Kee Yi, Sitansu Sekhar Nanda
Several studies have concluded that it is important to reduce COVID-19 severity using HCQ and CQ [53,71,72]. Similarly, 6–6.5 mg/kg per day dose of HCQ sulfate is quite safe and can lead to a serum level of 1.4–1.5 μM in humans, found to be effective for inhibiting SARS-CoV-2 infection [73]. The use of non-particulate CQ led to the synthesis of nanoparticles (NPs), which interfered with clathrin-mediated endocytosis of the virus and suppressed phosphatidylinositol-binding clathrin assembly protein (PICALM) to stop viral entry. This mechanism is responsible for the CQ-mediated effects on SARS-CoV-2 [74]. Liu et al. [73] reported that CQ and HCQ show faster oral absorption in humans with an almost analogous tissue distribution pattern, resulting in maximum drug concentrations in organs such as the spleen, kidney, liver, and lung, and reaching levels that are approximately 200–700 times greater than those in plasma. Despite promising activity against SARS-CoV-2, the use of both CQ and HCQ has been accompanied with a risk of arrhythmia in COVID-19 patients [75].