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Medicinal Plants Against COVID-19
Published in Hanadi Talal Ahmedah, Muhammad Riaz, Sagheer Ahmed, Marius Alexandru Moga, The Covid-19 Pandemic, 2023
Binish Khaliq, Naila Ali, Ahmed Akrem, M. Yasin Ashraf, Arif Malik, Arifa Tahir, M. Zia-Ul-Haq
COVID-19 used the ACE2 receptor as a bridge for transmission in humans. In 2020, Chen, and his colleagues demonstrated that spike glycoprotein of SARS-Coronavirus and COVID-19 has 72% structural similarities but SARS Coronavirus-2 RBD showed the better interaction with ACE2 as compare to the COVID-19 coronavirus [3]. ACE2 inhibitors take part to alter the binding site of RBD and mass infection caused by COVID-19. In addition, Wrapp and his colleagues [32] confirmed that spike protein of COVID-19 showed a higher similarity with ACE2 than SARS-Coronavirus [32]. Anti SARS drugs were used for blocking of SARS-Coronavirus with ACE2 inhibitors [33]. However, recent research has been shown that high blood pressure and diabetes remarkably provoked the infection chance of COVID-19 in the face of using Angiotensin-converting enzyme 2 (ACE2) inhibitors [34–36]. Ibuprofen, angiotensin II type-I receptor stoper, and Angiotensin-converting enzyme 2 (ACE2) inhibitors given on to ACE2 upregulation, which is need to use alternative ACE2 blockers [37].
AI and Immunology Considerations in Pandemics and SARS-CoV-2 COVID-19
Published in Louis J. Catania, AI for Immunology, 2021
The genomic data of the new coronavirus responsible for COVID-19 show that its spike protein contains some unique adaptations. One of these adaptations provides special ability of this coronavirus to bind to a specific protein on human cells called angiotensin converting enzyme (ACE-2). Human ACE-2 is expressed in epithelial cells of the lung and serve as an entry receptor site for SARS-CoV-2 spike glycoprotein.27 ACE-2 genetic polymorphism (occurrence of different forms in the life cycle of an individual organism) represented by diverse genetic variants in the human genome has been shown to affect virus-binding activity28 suggesting a possible genetic predisposition to COVID-19 infection. Thus, machine learning analysis of genetic variants from asymptomatic, mild, or severe COVID-19 patients can be performed to classify and predict people based on their vulnerability or resistance to potential COVID-19 infection. Furthermore, the machine learning model can also return those prioritized genetic variants, such as ACE-2 polymorphism.
Clinical Basis of COVID-19
Published in Wenguang Xia, Xiaolin Huang, Rehabilitation from COVID-19, 2021
How does the 2019-nCoV work? The spike protein (S protein) on the surface of the virus enters the host cell by interacting with specific receptors on the cell surface. Then it enters the cell through membrane fusion and releases its genome into the cytoplasm. The virus mainly binds to angiotensin-converting enzyme 2 (ACE2) via the S protein on its surface. During fusion, the S protein undergoes structural rearrangement to fuse the viral membrane with the host cell membrane, thereby infecting human respiratory epithelial cells. It has a higher affinity than SARS-CoV and, therefore, is more infectious.
Myocarditis: causes, mechanisms, and evolving therapies
Published in Expert Opinion on Therapeutic Targets, 2023
Tin Kyaw, Grant Drummond, Alex Bobik, Karlheinz Peter
SARS-CoV-2 (COVID-19): Several monoclonal antibodies have recently been introduced to treat infected patients [121]. Like vaccines, drug development has largely targeted the Spike protein, which forms homotrimers protruding from the viral surface that mediates coronavirus entry into host cells when it binds to ACE2 [122]. Antibodies include a neutralizing human antibody that binds to the N-terminal domain of the spike protein [123]. Other antibodies target the spike protein receptor-binding domain [124]. A major issue in just targeting the spike protein is the high frequency of mutations that may result in the loss of antibody inhibitory activity [125]. To date, more than 80 natural variants and 26 glycosylation spike mutants have been identified that can influence virus infectivity and antigenicity [126]. Current emerging omicron sublineages appear resistant to most clinically used antibodies [121], requiring combination with additional treatment options.
Very severe immune aplastic anemia after mRNA vaccination against COVID-19 responds well to immunosuppressive therapy: clinical characteristics and comparison to previous reports
Published in Hematology, 2022
Suhyeon Woo, Bohyun Kim, Sang-Cheol Lee, Min-Sun Kim, Young Ahn Yoon, Young-Jin Choi
Until now, several hematologic adverse effects from COVID-19 vaccinations have been reported, with variable severity and outcomes [1–7,9,10]. The precise cause of hematologic adverse effects, mostly cytopenia, is currently unclear. However, most studies have suggested an underlying immunologic mechanism [2–4,6,14,15]. The triggering of autoimmune responses to host proteins has been considered a mechanism in the development of COVID-19 vaccine-induced thrombotic thrombocytopenia [6]. A similar mechanism of AA after COVID-19 vaccination was proposed in previous reports [1,11]. The current literature revealed a few hypotheses regarding the relationship between spike protein received in mRNA vaccines and adverse effects [16]. There are possible interactions between spike protein and several intra-/extracellular signaling pathways, which result in various post-vaccination adverse effects [16]. According to proteomic analysis, severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2) spike protein could bind to hemoglobin and its metabolites, and lead to further adverse medical diseases [16,17]. A previous study reported a possible association between AA relapse and COVID-19 vaccination [12]. In that study, enhanced CD8+ T-cell-dependent activation and immune-mediated response to an mRNA-based COVID-19 vaccine were suggested as mechanisms for the increased AA relapse risk.
Histopathology of Third Trimester Placenta from SARS-CoV-2-Positive Women
Published in Fetal and Pediatric Pathology, 2022
Mai He, Priya Skaria, Kasey Kreutz, Ling Chen, Ian S. Hagemann, Ebony B. Carter, Indira U. Mysorekar, D. Michael Nelson, John Pfeifer, Louis P. Dehner
Coronavirus disease 2019 (COVID-19) is caused by infection of SARS-CoV-2, a member of the betacoronavirus family. SARS-CoV-2 is a 30 kb enveloped, positive sense, single-stranded RNA virus. The virus consists of four structural proteins (spike surface glycoprotein, envelope protein, membrane protein, and nucleocapsid protein) and nonstructural proteins. The spike protein consists of two functional subunits. The S1 subunit is responsible for binding to the host cell receptor and the S2 subunit is utilized for the fusion of the viral and cellular membranes [1, 2]. Studies showed that the spike protein for SARS-CoV-2 binds to angiotensin converting enzyme 2 (ACE2), which is also a functional receptor for SARS-CoV. ACE2 expression is high in lung, heart, ileum, kidney and bladder. Thus, SARS-CoV-2 virus primarily affects the respiratory system, although other organ systems may also be involved [1].