Cell-cell fusion induced by reovirus FAST proteins enhances replication and pathogenicity of non-enveloped dsRNA viruses
Fusogenic reoviruses encode fusion-associated small transmembrane (FAST) protein, which induces cell-cell fusion. FAST protein is the only known fusogenic protein in non-enveloped viruses, and its role in virus replication is not yet known. We generated replication-competent, FAST protein-deficient...
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| Veröffentlicht in: | PLoS pathogens 2019-04, Vol.15 (4), p.e1007675 |
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| creator | Kanai, Yuta Kawagishi, Takahiro Sakai, Yusuke Nouda, Ryotaro Shimojima, Masayuki Saijo, Masayuki Matsuura, Yoshiharu Kobayashi, Takeshi |
| description | Fusogenic reoviruses encode fusion-associated small transmembrane (FAST) protein, which induces cell-cell fusion. FAST protein is the only known fusogenic protein in non-enveloped viruses, and its role in virus replication is not yet known. We generated replication-competent, FAST protein-deficient pteropine orthoreovirus and demonstrated that FAST protein was not essential for viral replication, but enhanced viral replication in the early phase of infection. Addition of recombinant FAST protein enhanced replication of FAST-deficient virus and other non-fusogenic viruses in a fusion-dependent and FAST-species-independent manner. In a mouse model, replication and pathogenicity of FAST-deficient virus were severely impaired relative to wild-type virus, indicating that FAST protein is a major determinant of the high pathogenicity of fusogenic reovirus. FAST-deficient virus also conferred effective protection against challenge with lethal homologous virus strains in mice. Our results demonstrate a novel role of a viral fusogenic protein and the existence of a cell-cell fusion-dependent replication system in non-enveloped viruses. |
| doi_str_mv | 10.1371/journal.ppat.1007675 |
| format | Article |
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FAST protein is the only known fusogenic protein in non-enveloped viruses, and its role in virus replication is not yet known. We generated replication-competent, FAST protein-deficient pteropine orthoreovirus and demonstrated that FAST protein was not essential for viral replication, but enhanced viral replication in the early phase of infection. Addition of recombinant FAST protein enhanced replication of FAST-deficient virus and other non-fusogenic viruses in a fusion-dependent and FAST-species-independent manner. In a mouse model, replication and pathogenicity of FAST-deficient virus were severely impaired relative to wild-type virus, indicating that FAST protein is a major determinant of the high pathogenicity of fusogenic reovirus. FAST-deficient virus also conferred effective protection against challenge with lethal homologous virus strains in mice. Our results demonstrate a novel role of a viral fusogenic protein and the existence of a cell-cell fusion-dependent replication system in non-enveloped viruses.</description><identifier>ISSN: 1553-7374</identifier><identifier>ISSN: 1553-7366</identifier><identifier>EISSN: 1553-7374</identifier><identifier>DOI: 10.1371/journal.ppat.1007675</identifier><identifier>PMID: 31022290</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Arthritis ; Biology and Life Sciences ; Cell Fusion ; Double-stranded RNA ; Encephalitis ; FAST protein ; Funding ; Fusion protein ; Fusion proteins ; Glycoproteins ; Homology ; Infection ; Infections ; Infectious diseases ; Male ; Medicine and Health Sciences ; Mice ; Mice, Inbred C3H ; Mutation ; Pathogenicity ; Pathogens ; Physiological aspects ; Plasmids ; Pneumonia ; Proteins ; Reoviridae - genetics ; Reoviridae - pathogenicity ; Reoviridae Infections - genetics ; Reoviridae Infections - metabolism ; Reoviridae Infections - virology ; Replication ; Research and Analysis Methods ; Risk factors ; Rotavirus infections ; Veterinary medicine ; Viral Fusion Proteins - genetics ; Viral Fusion Proteins - metabolism ; Virology ; Virulence ; Virus Replication ; Viruses</subject><ispartof>PLoS pathogens, 2019-04, Vol.15 (4), p.e1007675</ispartof><rights>COPYRIGHT 2019 Public Library of Science</rights><rights>2019 Kanai et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PLoS pathogens</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kanai, Yuta</au><au>Kawagishi, Takahiro</au><au>Sakai, Yusuke</au><au>Nouda, Ryotaro</au><au>Shimojima, Masayuki</au><au>Saijo, Masayuki</au><au>Matsuura, Yoshiharu</au><au>Kobayashi, Takeshi</au><au>Danthi, Pranav</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cell-cell fusion induced by reovirus FAST proteins enhances replication and pathogenicity of non-enveloped dsRNA viruses</atitle><jtitle>PLoS pathogens</jtitle><addtitle>PLoS Pathog</addtitle><date>2019-04-25</date><risdate>2019</risdate><volume>15</volume><issue>4</issue><spage>e1007675</spage><pages>e1007675-</pages><issn>1553-7374</issn><issn>1553-7366</issn><eissn>1553-7374</eissn><abstract>Fusogenic reoviruses encode fusion-associated small transmembrane (FAST) protein, which induces cell-cell fusion. FAST protein is the only known fusogenic protein in non-enveloped viruses, and its role in virus replication is not yet known. We generated replication-competent, FAST protein-deficient pteropine orthoreovirus and demonstrated that FAST protein was not essential for viral replication, but enhanced viral replication in the early phase of infection. Addition of recombinant FAST protein enhanced replication of FAST-deficient virus and other non-fusogenic viruses in a fusion-dependent and FAST-species-independent manner. In a mouse model, replication and pathogenicity of FAST-deficient virus were severely impaired relative to wild-type virus, indicating that FAST protein is a major determinant of the high pathogenicity of fusogenic reovirus. FAST-deficient virus also conferred effective protection against challenge with lethal homologous virus strains in mice. Our results demonstrate a novel role of a viral fusogenic protein and the existence of a cell-cell fusion-dependent replication system in non-enveloped viruses.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>31022290</pmid><doi>10.1371/journal.ppat.1007675</doi><orcidid>https://orcid.org/0000-0003-0531-8256</orcidid><orcidid>https://orcid.org/0000-0002-5532-207X</orcidid><orcidid>https://orcid.org/0000-0001-5458-7298</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Arthritis Biology and Life Sciences Cell Fusion Double-stranded RNA Encephalitis FAST protein Funding Fusion protein Fusion proteins Glycoproteins Homology Infection Infections Infectious diseases Male Medicine and Health Sciences Mice Mice, Inbred C3H Mutation Pathogenicity Pathogens Physiological aspects Plasmids Pneumonia Proteins Reoviridae - genetics Reoviridae - pathogenicity Reoviridae Infections - genetics Reoviridae Infections - metabolism Reoviridae Infections - virology Replication Research and Analysis Methods Risk factors Rotavirus infections Veterinary medicine Viral Fusion Proteins - genetics Viral Fusion Proteins - metabolism Virology Virulence Virus Replication Viruses |
| title | Cell-cell fusion induced by reovirus FAST proteins enhances replication and pathogenicity of non-enveloped dsRNA viruses |
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