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      Elevation in sphingolipid upon SARS-CoV-2 infection: possible implications for COVID-19 pathology

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          SARS-CoV-2 infection alters the levels of sphingolipids early post infection. This phenomenon is reflected by increased levels of sphingolipids, including gangliosides, in infected cells, as well as in serum in a SARS-CoV-2 murine model.

          Abstract

          Understanding pathways that might impact coronavirus disease 2019 (COVID-19) manifestations and disease outcomes is necessary for better disease management and for therapeutic development. Here, we analyzed alterations in sphingolipid (SL) levels upon infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2 infection induced elevation of SL levels in both cells and sera of infected mice. A significant increase in glycosphingolipid levels was induced early post SARS-CoV-2 infection, which was essential for viral replication. This elevation could be reversed by treatment with glucosylceramide synthase inhibitors. Levels of sphinganine, sphingosine, GA1, and GM3 were significantly increased in both cells and the murine model upon SARS-CoV-2 infection. The potential involvement of SLs in COVID-19 pathology is discussed.

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          A pneumonia outbreak associated with a new coronavirus of probable bat origin

          Peng Zhou, Xing-Lou Yang, Xian-Guang Wang … (2020)
          Since the outbreak of severe acute respiratory syndrome (SARS) 18 years ago, a large number of SARS-related coronaviruses (SARSr-CoVs) have been discovered in their natural reservoir host, bats 1–4 . Previous studies have shown that some bat SARSr-CoVs have the potential to infect humans 5–7 . Here we report the identification and characterization of a new coronavirus (2019-nCoV), which caused an epidemic of acute respiratory syndrome in humans in Wuhan, China. The epidemic, which started on 12 December 2019, had caused 2,794 laboratory-confirmed infections including 80 deaths by 26 January 2020. Full-length genome sequences were obtained from five patients at an early stage of the outbreak. The sequences are almost identical and share 79.6% sequence identity to SARS-CoV. Furthermore, we show that 2019-nCoV is 96% identical at the whole-genome level to a bat coronavirus. Pairwise protein sequence analysis of seven conserved non-structural proteins domains show that this virus belongs to the species of SARSr-CoV. In addition, 2019-nCoV virus isolated from the bronchoalveolar lavage fluid of a critically ill patient could be neutralized by sera from several patients. Notably, we confirmed that 2019-nCoV uses the same cell entry receptor—angiotensin converting enzyme II (ACE2)—as SARS-CoV.
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            COVID-19 and cardiovascular disease: from basic mechanisms to clinical perspectives

            Masataka Nishiga, Dao Wen Wang, Yaling Han … (2020)
            Coronavirus disease 2019 (COVID-19), caused by a strain of coronavirus known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a global pandemic that has affected the lives of billions of individuals. Extensive studies have revealed that SARS-CoV-2 shares many biological features with SARS-CoV, the zoonotic virus that caused the 2002 outbreak of severe acute respiratory syndrome, including the system of cell entry, which is triggered by binding of the viral spike protein to angiotensin-converting enzyme 2. Clinical studies have also reported an association between COVID-19 and cardiovascular disease. Pre-existing cardiovascular disease seems to be linked with worse outcomes and increased risk of death in patients with COVID-19, whereas COVID-19 itself can also induce myocardial injury, arrhythmia, acute coronary syndrome and venous thromboembolism. Potential drug–disease interactions affecting patients with COVID-19 and comorbid cardiovascular diseases are also becoming a serious concern. In this Review, we summarize the current understanding of COVID-19 from basic mechanisms to clinical perspectives, focusing on the interaction between COVID-19 and the cardiovascular system. By combining our knowledge of the biological features of the virus with clinical findings, we can improve our understanding of the potential mechanisms underlying COVID-19, paving the way towards the development of preventative and therapeutic solutions.
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              Sphingolipids and their metabolism in physiology and disease

              Yusuf Hannun, Lina M. Obeid (2017)
              Studies of bioactive lipids in general and sphingolipids in particular have intensified over the past several years, revealing an unprecedented and unanticipated complexity of the lipidome and its many functions, which rivals, if not exceeds, that of the genome or proteome. These results highlight critical roles for bioactive sphingolipids in most, if not all, major cell biological responses, including all major cell signalling pathways, and they link sphingolipid metabolism to key human diseases. Nevertheless, the fairly nascent field of bioactive sphingolipids still faces challenges in its biochemical and molecular underpinnings, including defining the molecular mechanisms of pathway and enzyme regulation, the study of lipid-protein interactions and the development of cellular probes, suitable biomarkers and therapeutic approaches.
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                Author and article information

                Contributors
                Einat B Vitner:
                ORCID: https://orcid.org/0000-0001-8578-8551
                Role: ConceptualizationRole: Formal analysisRole: SupervisionRole: Funding acquisitionRole: Writing—original draft, review, and editing
                Roy Avraham:
                ORCID: https://orcid.org/0000-0002-3010-3372
                Role: Data curationRole: Writing—review and editing
                Boaz Politi: Role: Data curation
                Sharon Melamed: Role: Data curation
                Tomer Israely:
                ORCID: https://orcid.org/0000-0003-0246-4477
                Role: ConceptualizationRole: Writing—review and editing
                Journal
                Journal ID (nlm-ta): Life Sci Alliance
                Journal ID (iso-abbrev): Life Sci Alliance
                Journal ID (hwp): lsa
                Journal ID (publisher-id): lsa
                Title: Life Science Alliance
                Publisher: Life Science Alliance LLC
                ISSN (Electronic): 2575-1077
                Publication date (Electronic): 11 November 2021
                Publication date Collection: January 2022
                Publication date PMC-release: 11 November 2021
                Volume: 5
                Issue: 1
                Electronic Location Identifier: e202101168
                Affiliations
                [1] Departments of Infectious Diseases, Israel Institute for Biological Research, Ness-Ziona, Israel
                Author notes
                Author information
                https://orcid.org/0000-0001-8578-8551
                https://orcid.org/0000-0002-3010-3372
                https://orcid.org/0000-0003-0246-4477
                Article
                Publisher ID: LSA-2021-01168
                DOI: 10.26508/lsa.202101168
                PMC ID: 8605327
                PubMed ID: 34764206
                SO-VID: 6521fd37-e5f4-46f7-ac46-780d07925e5e
                Copyright © © 2021 Vitner et al.
                License:

                This article is available under a Creative Commons License (Attribution 4.0 International, as described at https://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 23 July 2021
                Date revision received : 25 October 2021
                Date accepted : 26 October 2021
                Funding
                Funded by: Israel Science Foundation (ISF).;
                Award ID: Vitner EB 521/18
                Categories
                Subject: Resource
                Subject: Resources
                Subject: 14
                Subject: 16

                Data availability:

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