Viral apoptotic mimicry
Viral apoptotic mimicry, defined by the exposure of phosphatidylserine on the pathogen surface, is emerging as a common theme used by enveloped viruses to promote infection. In this Progress article, Amara and Mercer discuss how viruses acquire phosphatidylserine and how this mimicry might facilitat...
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| Veröffentlicht in: | Nature reviews. Microbiology 2015-08, Vol.13 (8), p.461-469 |
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| creator | Amara, Ali Mercer, Jason |
| description | Viral apoptotic mimicry, defined by the exposure of phosphatidylserine on the pathogen surface, is emerging as a common theme used by enveloped viruses to promote infection. In this Progress article, Amara and Mercer discuss how viruses acquire phosphatidylserine and how this mimicry might facilitate cell entry and evasion of the immune response.
As opportunistic pathogens, viruses have evolved many elegant strategies to manipulate host cells for infectious entry and replication. Viral apoptotic mimicry, defined by the exposure of phosphatidylserine — a marker for apoptosis — on the pathogen surface, is emerging as a common theme used by enveloped viruses to promote infection. Focusing on the four best described examples (vaccinia virus, dengue virus, Ebola virus and pseudotyped lentivirus), we summarize our current understanding of apoptotic mimicry as a mechanism for virus entry, binding and immune evasion. We also describe recent examples of non-enveloped viruses that use this mimicry strategy, and discuss future directions and how viral apoptotic mimicry could be targeted therapeutically. |
| doi_str_mv | 10.1038/nrmicro3469 |
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As opportunistic pathogens, viruses have evolved many elegant strategies to manipulate host cells for infectious entry and replication. Viral apoptotic mimicry, defined by the exposure of phosphatidylserine — a marker for apoptosis — on the pathogen surface, is emerging as a common theme used by enveloped viruses to promote infection. Focusing on the four best described examples (vaccinia virus, dengue virus, Ebola virus and pseudotyped lentivirus), we summarize our current understanding of apoptotic mimicry as a mechanism for virus entry, binding and immune evasion. We also describe recent examples of non-enveloped viruses that use this mimicry strategy, and discuss future directions and how viral apoptotic mimicry could be targeted therapeutically.</description><identifier>ISSN: 1740-1526</identifier><identifier>EISSN: 1740-1534</identifier><identifier>DOI: 10.1038/nrmicro3469</identifier><identifier>PMID: 26052667</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/326/596/1413 ; 631/326/596/1746 ; 631/326/596/2042 ; 631/326/596/2116 ; 631/326/596/2557 ; 631/326/596/2558 ; 631/80/82/23 ; Animals ; Apoptosis ; Apoptosis - physiology ; Dengue fever ; Dengue virus ; Dengue viruses ; Ebola virus ; Health aspects ; Humans ; Immune Evasion ; Immune response ; Immune system ; Infection ; Infectious Diseases ; Lentivirus ; Life Sciences ; Marburg virus disease ; Medical Microbiology ; Microbiology ; Mimicry ; Mimicry (Biology) ; Molecular Mimicry ; Opportunist infection ; Parasitology ; Pathogens ; Phagocytes - metabolism ; Phosphatidylserine ; Phosphatidylserines - metabolism ; Phospholipids ; Practice ; progress ; Receptors, Cell Surface - physiology ; Vaccinia virus ; Vector-borne diseases ; Viral diseases ; Viral research ; Virology ; Virus Internalization ; Viruses ; Viruses - immunology ; Viruses - metabolism</subject><ispartof>Nature reviews. Microbiology, 2015-08, Vol.13 (8), p.461-469</ispartof><rights>Springer Nature Limited 2015</rights><rights>COPYRIGHT 2015 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Aug 2015</rights><rights>Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c672t-e4f7d39a7df0104861c110b6a8532d707f6ae813fd5d277ab87d5a4a85da3b6f3</citedby><cites>FETCH-LOGICAL-c672t-e4f7d39a7df0104861c110b6a8532d707f6ae813fd5d277ab87d5a4a85da3b6f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/nrmicro3469$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/nrmicro3469$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26052667$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Amara, Ali</creatorcontrib><creatorcontrib>Mercer, Jason</creatorcontrib><title>Viral apoptotic mimicry</title><title>Nature reviews. Microbiology</title><addtitle>Nat Rev Microbiol</addtitle><addtitle>Nat Rev Microbiol</addtitle><description>Viral apoptotic mimicry, defined by the exposure of phosphatidylserine on the pathogen surface, is emerging as a common theme used by enveloped viruses to promote infection. In this Progress article, Amara and Mercer discuss how viruses acquire phosphatidylserine and how this mimicry might facilitate cell entry and evasion of the immune response.
As opportunistic pathogens, viruses have evolved many elegant strategies to manipulate host cells for infectious entry and replication. Viral apoptotic mimicry, defined by the exposure of phosphatidylserine — a marker for apoptosis — on the pathogen surface, is emerging as a common theme used by enveloped viruses to promote infection. Focusing on the four best described examples (vaccinia virus, dengue virus, Ebola virus and pseudotyped lentivirus), we summarize our current understanding of apoptotic mimicry as a mechanism for virus entry, binding and immune evasion. We also describe recent examples of non-enveloped viruses that use this mimicry strategy, and discuss future directions and how viral apoptotic mimicry could be targeted therapeutically.</description><subject>631/326/596/1413</subject><subject>631/326/596/1746</subject><subject>631/326/596/2042</subject><subject>631/326/596/2116</subject><subject>631/326/596/2557</subject><subject>631/326/596/2558</subject><subject>631/80/82/23</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - physiology</subject><subject>Dengue fever</subject><subject>Dengue virus</subject><subject>Dengue viruses</subject><subject>Ebola virus</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Immune Evasion</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Infection</subject><subject>Infectious Diseases</subject><subject>Lentivirus</subject><subject>Life Sciences</subject><subject>Marburg virus disease</subject><subject>Medical Microbiology</subject><subject>Microbiology</subject><subject>Mimicry</subject><subject>Mimicry (Biology)</subject><subject>Molecular Mimicry</subject><subject>Opportunist infection</subject><subject>Parasitology</subject><subject>Pathogens</subject><subject>Phagocytes - 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Microbiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Amara, Ali</au><au>Mercer, Jason</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Viral apoptotic mimicry</atitle><jtitle>Nature reviews. Microbiology</jtitle><stitle>Nat Rev Microbiol</stitle><addtitle>Nat Rev Microbiol</addtitle><date>2015-08-01</date><risdate>2015</risdate><volume>13</volume><issue>8</issue><spage>461</spage><epage>469</epage><pages>461-469</pages><issn>1740-1526</issn><eissn>1740-1534</eissn><abstract>Viral apoptotic mimicry, defined by the exposure of phosphatidylserine on the pathogen surface, is emerging as a common theme used by enveloped viruses to promote infection. In this Progress article, Amara and Mercer discuss how viruses acquire phosphatidylserine and how this mimicry might facilitate cell entry and evasion of the immune response.
As opportunistic pathogens, viruses have evolved many elegant strategies to manipulate host cells for infectious entry and replication. Viral apoptotic mimicry, defined by the exposure of phosphatidylserine — a marker for apoptosis — on the pathogen surface, is emerging as a common theme used by enveloped viruses to promote infection. Focusing on the four best described examples (vaccinia virus, dengue virus, Ebola virus and pseudotyped lentivirus), we summarize our current understanding of apoptotic mimicry as a mechanism for virus entry, binding and immune evasion. We also describe recent examples of non-enveloped viruses that use this mimicry strategy, and discuss future directions and how viral apoptotic mimicry could be targeted therapeutically.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>26052667</pmid><doi>10.1038/nrmicro3469</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 631/326/596/1413 631/326/596/1746 631/326/596/2042 631/326/596/2116 631/326/596/2557 631/326/596/2558 631/80/82/23 Animals Apoptosis Apoptosis - physiology Dengue fever Dengue virus Dengue viruses Ebola virus Health aspects Humans Immune Evasion Immune response Immune system Infection Infectious Diseases Lentivirus Life Sciences Marburg virus disease Medical Microbiology Microbiology Mimicry Mimicry (Biology) Molecular Mimicry Opportunist infection Parasitology Pathogens Phagocytes - metabolism Phosphatidylserine Phosphatidylserines - metabolism Phospholipids Practice progress Receptors, Cell Surface - physiology Vaccinia virus Vector-borne diseases Viral diseases Viral research Virology Virus Internalization Viruses Viruses - immunology Viruses - metabolism |
| title | Viral apoptotic mimicry |
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