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Order Nidovirales
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
In contrast to the well-known human betacoronaviruses that are described later, the human alphacoronaviruses including human coronavirus NL63 (HCoV-NL63) cause mainly mild infections of the upper respiratory tract (van der Hoek et al. 2004), while SARS-CoV, MERS-CoV, and SARS-CoV-2 are responsible for severe disease with high morbidity and mortality rate, as reviewed by Vellingiri et al. (2020). Moreover, the importance of the studies in human alphacoronaviruses is growing due to the established facts that the preexisting HCoV-NL63 antibody response is cross reacting with SARS-CoV-2 (Simula et al. 2020). It was suggested accordingly by the authors that the previous exposure to HCoV-NL63 epitopes would produce antibodies that could confer a protective immunity against SARS-CoV-2 and probably reduce the severity of the disease.
SARS-CoV-2 Infection Dysregulates Host Iron (Fe)-Redox Homeostasis (Fe-R-H): Role of Fe-Redox Regulators, Ferroptosis Inhibitors, Anticoagulants, and Iron-Chelators in COVID-19 Control
Published in Journal of Dietary Supplements, 2023
Sreus A.G. Naidu, Roger A. Clemens, A. Satyanarayan Naidu
Caffeic acid is a plant-based iron-chelator, redox modulator, and a powerful natural antioxidant (330). Caffeic acid acts as both metal-chelator and hydrogen (H) donor to prevent harmful effects of lipid-derived peroxyl and alkoxyl radicals (lipid peroxidation) on biological membranes (Figure 7B) (331). Caffeic acid inhibits several viral pathogens such as the herpes simplex (HSV), influenza and immunodeficiency viruses (HIV) and its antiviral activity is potentiated >100-fold in the presence of iron. Caffeic chelates seem to target and interfere with viral attachment to heparan sulfate proteoglycans (HSPG) on cell surface (332). Caffeic acid effectively inhibits the replication of human coronavirus NL63 in a cell-type independent manner (IC50=3.54μM), and specifically blocks the viral attachment (IC50=8.1μM) (333). A phenethyl ester (from propolis) of caffeic acid is shown to interact with the substrate-binding pocket of SARS-CoV-2 Mpro with affinity and binding energies (ΔG= −4.79kcal/mole) comparable to N3 (ΔG= −5.68kcal/mole), the reference viral protease inhibitor (334). Several caffeic acid-derivatives (Khainaoside C, 6-O-Caffeoylarbutin, Khainaoside B, Khainaoside C and Vitexfolin A) demonstrate higher binding energies (ΔG) than the antiviral drug nelfinavir against COVID-19 Mpro, Nsp15, SARS-CoV-2 spike S2 subunit, spike open state and closed state structures. Caffeic acid forms H-bonds with Asn142 and Glu166 residues of SARS-CoV-2 Mpro enzyme (335).
Molecular detections of coronavirus: current and emerging methodologies
Published in Expert Review of Anti-infective Therapy, 2022
Mingkun Diao, Lang Lang, Juan Feng, Rongsong Li
The pandemic of coronavirus disease 2019 (COVID-19) caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has already claimed more than 3 million deaths worldwide so far. SARS-CoV-2 belongs to the genus Coronavirus, which widely exist in nature with positive-sense, single-stranded RNA as their genetic material. Seven coronaviruses have been identified to cause respiratory diseases in human, including human coronavirus 229E (HCoV-229E), human coronavirus OC43 (HCoV-OC43), human coronavirus NL63 (HCoV-NL63), human coronavirus HKU1 (HCoV-HKU1), Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV), Middle East Respiratory Syndrome Coronavirus (MERS-CoV), and SARS-CoV-2 [1]. In the past two decades, the spreading of coronavirus caused three epidemics with severe symptoms and high mortality rates in patients. The SARS-CoV in late 2002, upon identified in China, quickly spread to Southeast Asia and other regions in the world. This epidemic was gradually eliminated by mid-2003 and had a mortality rate around 10% [2]. The MERS-CoV outbreak was firstly identified in Saudi Arabia in September, 2012, and quickly spread to Mid-east Asia, Europe, North America, and Southeast Asia, then ended in May, 2015. It had more than 1000 confirmed cases with a striking mortality rate of more than 35% [3]. The recent SARS-CoV-2 pandemic started in late 2019 [4]. Though the fatality rate for the ongoing pandemic is less as compared to SARS and MERS, it is much more contagious and led to far more total deaths [5].
Pathogenesis guided therapeutic management of COVID-19: an immunological perspective
Published in International Reviews of Immunology, 2021
Ashutosh Kumar, Pranav Prasoon, Prakash S. Sekhawat, Vikas Pareek, Muneeb A. Faiq, Chiman Kumari, Ravi K. Narayan, Maheswari Kulandhasamy, Kamla Kant
Prophylactic dose of low molecular weight heparin (LMWH) may be advisable for hospitalized patients and treatment dose LMWH is contemplated for those with significantly raised D-dimer concentrations [100]. LMWH also has anti-inflammatory properties that might be protective. Owing to the possible involvement of proteinase-activated receptors (PARs) in thrombosis, PAR antagonists and other coagulation protease inhibitors may have some beneficial role in preventing thrombosis [66]. Some authors suggested use of unfractionated heparin (UH) where disseminated intravascular coagulation (DIC) is threatened, or fibrinolytics like tissue plasminogen activation (tPA) inhibitors as a salvage therapy when clotting has already taken place. Existing evidence for the antiviral properties of heparin against coronaviruses like SARS-CoV-1and human coronavirus NL63 (HCoV-NL63) suggested comparative benefits of using heparin (however any direct proof for its antiviral property against SARS-CoV-2 is lacking for now) [101,102].