Inviting an author to review:
Find an author and click ‘Invite to review selected article’ near their name.
Search for authorsSearch for similar articles
14
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Eph receptors: the bridge linking host and virus

      review-article

      Read this article at

      Bookmark
          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

          Eph (erythropoietin-producing hepatoma) receptors and Ephrin ligands constitute the largest subfamily of receptor tyrosine kinase (RTK), which were first discovered in tumors. Heretofore, Eph protein has been shown to be involved in various tumor biological behaviors including proliferation and progression. The occurrence of specific types of tumor is closely related to the virus infection. Virus entry is a complex process characterized by a series of events. The entry into target cells is an essential step for virus to cause diseases, which requires the fusion of the viral envelope and host cellular membrane mediated by viral glycoproteins and cellular receptors. Integrin molecules are well known as entry receptors for most herpes viruses. However, in recent years, Eph receptors and their Ephrin ligands have been reported to be involved in virus infections. The main mechanism may be the interaction between Eph receptors and conserved viral surface glycoprotein, such as the gH/gL or gB protein of the herpesviridae. This review focuses on the relationship between Eph receptor family and virus infection that summarize the processes of viruses such as EBV, KSHV, HCV, RRV, etc., infecting target cells through Eph receptors and activating its downstream signaling pathways resulting in malignancies. Finally, we discussed the perspectives to block virus infection, prevention, and treatment of viral-related tumors via Eph receptor family.

          Related collections

          Most cited references91

          • Record: found
          • Abstract: found
          • Article: not found

          Evolutionary and biomedical insights from the rhesus macaque genome.

          The rhesus macaque (Macaca mulatta) is an abundant primate species that diverged from the ancestors of Homo sapiens about 25 million years ago. Because they are genetically and physiologically similar to humans, rhesus monkeys are the most widely used nonhuman primate in basic and applied biomedical research. We determined the genome sequence of an Indian-origin Macaca mulatta female and compared the data with chimpanzees and humans to reveal the structure of ancestral primate genomes and to identify evidence for positive selection and lineage-specific expansions and contractions of gene families. A comparison of sequences from individual animals was used to investigate their underlying genetic diversity. The complete description of the macaque genome blueprint enhances the utility of this animal model for biomedical research and improves our understanding of the basic biology of the species.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Binding of hepatitis C virus to CD81.

            Chronic hepatitis C virus (HCV) infection occurs in about 3 percent of the world's population and is a major cause of liver disease. HCV infection is also associated with cryoglobulinemia, a B lymphocyte proliferative disorder. Virus tropism is controversial, and the mechanisms of cell entry remain unknown. The HCV envelope protein E2 binds human CD81, a tetraspanin expressed on various cell types including hepatocytes and B lymphocytes. Binding of E2 was mapped to the major extracellular loop of CD81. Recombinant molecules containing this loop bound HCV and antibodies that neutralize HCV infection in vivo inhibited virus binding to CD81 in vitro.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The human scavenger receptor class B type I is a novel candidate receptor for the hepatitis C virus.

              We discovered that the hepatitis C virus (HCV) envelope glycoprotein E2 binds to human hepatoma cell lines independently of the previously proposed HCV receptor CD81. Comparative binding studies using recombinant E2 from the most prevalent 1a and 1b genotypes revealed that E2 recognition by hepatoma cells is independent from the viral isolate, while E2-CD81 interaction is isolate specific. Binding of soluble E2 to human hepatoma cells was impaired by deletion of the hypervariable region 1 (HVR1), but the wild-type phenotype was recovered by introducing a compensatory mutation reported previously to rescue infectivity of an HVR1-deleted HCV infectious clone. We have identified the receptor responsible for E2 binding to human hepatic cells as the human scavenger receptor class B type I (SR-BI). E2-SR-BI interaction is very selective since neither mouse SR-BI nor the closely related human scavenger receptor CD36, were able to bind E2. Finally, E2 recognition by SR-BI was competed out in an isolate-specific manner both on the hepatoma cell line and on the human SR-BI-transfected cell line by an anti-HVR1 monoclonal antibody.
                Bookmark

                Author and article information

                Contributors
                474044435@qq.com
                qinzailong@hotmail.com
                Journal
                Cell Mol Life Sci
                Cell. Mol. Life Sci
                Cellular and Molecular Life Sciences
                Springer International Publishing (Cham )
                1420-682X
                1420-9071
                31 December 2019
                31 December 2019
                2020
                : 77
                : 12
                : 2355-2365
                Affiliations
                [1 ]GRID grid.254020.1, ISNI 0000 0004 1798 4253, Department of Immunology, , Changzhi Medical College, ; Changzhi, 046000 Shanxi China
                [2 ]GRID grid.443385.d, ISNI 0000 0004 1798 9548, Department of Pathology, Affiliated Hospital of Guilin Medical University, ; Guilin, 541001 Guangxi China
                [3 ]GRID grid.216417.7, ISNI 0000 0001 0379 7164, School of Basic Medical Science, Cancer Research Institute, , Central South University, ; Changsha, 410008 Hunan China
                [4 ]GRID grid.410649.e, Laboratory of Genetics and Metabolism, , Maternal and Child Health Hospital of Guangxi Zhuang Autonomous Region, Guangxi Birth Defects Research And Prevention Institute, ; Nanning, 530003 Guangxi China
                Author information
                http://orcid.org/0000-0001-7109-6693
                Article
                3409
                10.1007/s00018-019-03409-6
                7275029
                31893311
                47acea39-6c23-482c-895f-c01021aa15d7
                © The Author(s) 2019

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 13 June 2019
                : 17 November 2019
                : 2 December 2019
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;
                Award ID: 81702919
                Award ID: 81802478
                Award Recipient :
                Funded by: Guangxi Natural Science Foundation
                Award ID: 2017JJB10161
                Award ID: 2018JJB140315
                Award Recipient :
                Categories
                Review
                Custom metadata
                © Springer Nature Switzerland AG 2020

                Molecular biology
                eph receptor,virus infection,virus-associated cancer,ebv,kshv
                Molecular biology
                eph receptor, virus infection, virus-associated cancer, ebv, kshv

                Comments

                Comment on this article

                scite_
                0
                0
                0
                0
                Smart Citations
                0
                0
                0
                0
                Citing PublicationsSupportingMentioningContrasting
                View Citations

                See how this article has been cited at scite.ai

                scite shows how a scientific paper has been cited by providing the context of the citation, a classification describing whether it supports, mentions, or contrasts the cited claim, and a label indicating in which section the citation was made.

                Similar content434

                Cited by16

                Most referenced authors2,215