SARS-CoV-2: A comprehensive review from pathogenicity of the virus to clinical consequences.
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ABSTRACT:
SUBMITTER: Lotfi M
PROVIDER: S-EPMC7300719 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The coronavirus disease (COVID-19) was first identified in China, December 2019. Since then, it has spread the length and breadth of the world at an unprecedented, alarming rate. Severe acute respiratory syndrome coronavirus (SARS-CoV)-2, which causes COVID-19, has much in common with its closest homologs, SARS-CoV and Middle East respiratory syndrome-CoV. The virus-host interaction of SARS-CoV-2 uses the same receptor, ACE2, which is similar to that of SARS-CoV, which spreads through the respiratory tract. Patients with COVID-19 report symptoms including mild-to-severe fever, cough and fatigue; very few patients report gastrointestinal infections. There are no specific antiviral strategies. A few strong medications are under investigation, so we have to focus on proposals which ought to be taken to forestall this infection in a living host.
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Project description:The current COVID-19 global pandemic poses immense challenges to global health, largely due to the difficulty to detect infection in the early stages of the disease, as well as the current lack of effective antiviral therapy. Research and understanding of the human immune system can provide important theoretical and technical support for the clinical diagnosis and treatment of COVID-19, the clinical implementations of which include immunoassays and immunotherapy, which play a crucial role in the fight against the pandemic. This review consolidates the current scientific evidence for immunoassay, which includes multiple methods of detecting antigen and antibody against SARS-CoV-2. We compared the characteristics, advantages and disadvantages, and clinical applications of these three detection techniques. In addition to detecting viral infections, knowledge on the body's immunity against the virus is desirable; thus, the immunotherapy-based neutralizing antibody (nAb) detection methods were discussed. We also gave a brief introduction to the new immunoassay technology such as biosensing. This was followed by an in-depth and extensive review on a variety of immunotherapy methods. It includes convalescent plasma therapy, neutralizing antibody-based treatments targeting different regions of SARS-CoV-2, immunotherapy targeted on the host cell including inhibiting the host cell receptor and cytokine storm, as well as cocktail antibodies, cross-neutralizing antibodies, and immunotherapy based on cross-reactivity between viral epitopes and autoepitopes and autoantibody. Despite the development of various immunological testing methods and antibody therapies, the current global situation of COVID-19 is still tense. We need more efficient detection methods and more reliable antibody therapies. The up-to-date knowledge on therapeutic strategies will likely help clinicians worldwide to protect patients from life-threatening viral infections.
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Project description:SARS-CoV-2 coronavirus is one of the largest RNA viruses (26-32kb) and has emerged as a major threat to global public health. The resulting pandemic has caused global societal and economic disruptions. Here, we investigate the intramolecular and intermolecular RNA interactions of wildtype and a 382 deletion SARS-CoV-2 virus inside cells. We identified twelve potentially functional structural elements along the SARS-CoV-2 genome and observed that subgenomic viral RNA (sgRNAs) contains different structures that could be important for their functions using direct RNA sequencing. Proximity ligation sequencing experiments identified hundreds of intramolecular and intermolecular pair-wise interactions within the virus genome and between virus and host cellular RNAs. SARS-CoV-2 binds strongly to mitochondrial and nucleolar RNAs including COX1 and SNORD27, and contains 130 2’O-methylation sites along its genome. 2’O-methylation sites along the virus RNA are enriched in the UTRs and associated with increased pair-wise interactions. SARS-CoV-2 infection also results in a global decrease of 2’O-methylation sites on host mRNAs, suggesting that binding of SARS-CoV-2 to snoRNAs could be a pro-viral mechanism to sequester methylation machinery away from host RNAs to methylate the virus genome. Collectively, these studies deepen our understanding of the molecular basis of SARS-CoV-2 pathogenicity, its cellular host factors and provides a platform for targeting the virus.
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Project description:Emerging and re-emerging viral diseases can create devastating effects on human lives and may also lead to economic crises. The ongoing COVID-19 pandemic due to the novel coronavirus (nCoV), severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which originated in Wuhan, China, has caused a global public health emergency. To date, the molecular mechanism of transmission of SARS-CoV-2, its clinical manifestations and pathogenesis is not completely understood. The global scientific community has intensified its efforts in understanding the biology of SARS-CoV-2 for development of vaccines and therapeutic interventions to prevent the rapid spread of the virus and to control mortality and morbidity associated with COVID-19. To understand the pathophysiology of SARS-CoV-2, appropriate animal models that mimic the biology of human SARS-CoV-2 infection are urgently needed. In this review, we outline animal models that have been used to study previous human coronaviruses (HCoVs), including severe acute respiratory syndrome coronavirus (SARS-CoV) and middle east respiratory syndrome coronavirus (MERS-CoV). Importantly, we discuss models that are appropriate for SARS-CoV-2 as well as the advantages and disadvantages of various available methods.
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Project description:Coronavirus disease 2019 (COVID-19), the disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been declared a global pandemic with significant morbidity and mortality since first appearing in Wuhan, China, in late 2019. As many countries are grappling with the onset of their epidemics, pharmacotherapeutics remain lacking. The window of opportunity to mitigate downstream morbidity and mortality is narrow but remains open. The renin-angiotensin-aldosterone system (RAAS) is crucial to the homeostasis of both the cardiovascular and respiratory systems. Importantly, SARS-CoV-2 utilises and interrupts this pathway directly, which could be described as the renin-angiotensin-aldosterone-SARS-CoV (RAAS-SCoV) axis. There exists significant controversy and confusion surrounding how anti-hypertensive agents might function along this pathway. This review explores the current state of knowledge regarding the RAAS-SCoV axis (informed by prior studies of SARS-CoV), how this relates to our currently evolving pandemic, and how these insights might guide our next steps in an evidence-based manner. This review discusses the role of the RAAS-SCoV axis in acute lung injury and the effects, risks and benefits of pharmacological modification of this axis. There may be an opportunity to leverage the different aspects of RAAS inhibitors to mitigate indirect viral-induced lung injury. Concerns have been raised that such modulation might exacerbate the disease. While relevant preclinical, experimental models to date favour a protective effect of RAAS-SCoV axis inhibition on both lung injury and survival, clinical data related to the role of RAAS modulation in the setting of SARS-CoV-2 remain limited. Proposed interventions for SARS-CoV-2 predominantly focus on viral microbiology and aim to inhibit viral cellular injury. While these therapies are promising, immediate use may not be feasible, and the time window of their efficacy remains a major unanswered question. An alternative approach is the modulation of the specific downstream pathophysiological effects caused by the virus that lead to morbidity and mortality. We propose a preponderance of evidence that supports clinical equipoise regarding the efficacy of RAAS-based interventions, and the imminent need for a multisite randomised controlled clinical trial to evaluate the inhibition of the RAAS-SCoV axis on acute lung injury in COVID-19.
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Project description:COVID-19, the disease caused by SARS-CoV-2, has claimed approximately 5 million lives and 257 million cases reported globally. This virus and disease have significantly affected people worldwide, whether directly and/or indirectly, with a virulent pathogen that continues to evolve as we race to learn how to prevent, control, or cure COVID-19. The focus of this review is on the SARS-CoV-2 virus' mechanism of infection and its proclivity at adapting and restructuring the intracellular environment to support viral replication. We highlight current knowledge and how scientific communities with expertize in viral, cellular, and clinical biology have contributed to increase our understanding of SARS-CoV-2, and how these findings may help explain the widely varied clinical observations of COVID-19 patients.
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Project description:Several studies have suggested a relationship between SARS-CoV-2 infection and diabetes. This study examined the consequences of infection of human pancreatic islets with SARS-CoV-2 virus. This GEO submission contains the raw and processed data from single-cell RNA sequencing (scRNAseq) experiments evaluating the tropism of SARS-CoV-2 in pancreatic islets and transcriptional changes induced by infection of these cells. Overall we observed limited infection of pancreatic islets (0.2 - 3.4% of all cells infected per donor) and identified multiple pancreatic cell types as targets of infection; due to the preponderance of major endocrine cell populations in our islet cell preparations, downstream analyses were primarily focused on alpha and beta cells. Within beta cells we identified an upregulation of interferon stimulated genes in both infected and bystander cells as well as an NFκB mediated genes in infected cells only. Within alpha cells we detected a non-specific downregulation of a large number of host genes in infected cells.
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