Enhanced growth of influenza A virus by coinfection with human parainfluenza virus type 2
It has been reported that dual or multiple viruses can coinfect epithelial cells of the respiratory tract. However, little has been reported on in vitro interactions of coinfected viruses. To explore how coinfection of different viruses affects their biological property, we examined growth of influe...
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Veröffentlicht in: | Medical microbiology and immunology 2016-06, Vol.205 (3), p.209-218 |
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description | It has been reported that dual or multiple viruses can coinfect epithelial cells of the respiratory tract. However, little has been reported on in vitro interactions of coinfected viruses. To explore how coinfection of different viruses affects their biological property, we examined growth of influenza A virus (IAV) and human parainfluenza virus type 2 (hPIV2) during coinfection of Vero cells. We found that IAV growth was enhanced by coinfection with hPIV2. The enhanced growth of IAV was not reproduced by coinfection with an hPIV2 mutant with reduced cell fusion activity, or by ectopic expression of the V protein of hPIV2. In contrast, induction of cell fusion by ectopic expression of the hPIV2 HN and F proteins augments IAV growth. hPIV2 coinfection supported IAV growth in cells originated from the respiratory epithelium. The enhancement correlated closely with cell fusion ability of hPIV2 in those cells. These results indicate that cell fusion induced by hPIV2 infection is beneficial to IAV replication and that enhanced viral replication by coinfection with different viruses can modify their pathological consequences. |
doi_str_mv | 10.1007/s00430-015-0441-y |
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However, little has been reported on in vitro interactions of coinfected viruses. To explore how coinfection of different viruses affects their biological property, we examined growth of influenza A virus (IAV) and human parainfluenza virus type 2 (hPIV2) during coinfection of Vero cells. We found that IAV growth was enhanced by coinfection with hPIV2. The enhanced growth of IAV was not reproduced by coinfection with an hPIV2 mutant with reduced cell fusion activity, or by ectopic expression of the V protein of hPIV2. In contrast, induction of cell fusion by ectopic expression of the hPIV2 HN and F proteins augments IAV growth. hPIV2 coinfection supported IAV growth in cells originated from the respiratory epithelium. The enhancement correlated closely with cell fusion ability of hPIV2 in those cells. These results indicate that cell fusion induced by hPIV2 infection is beneficial to IAV replication and that enhanced viral replication by coinfection with different viruses can modify their pathological consequences.</description><identifier>ISSN: 0300-8584</identifier><identifier>EISSN: 1432-1831</identifier><identifier>DOI: 10.1007/s00430-015-0441-y</identifier><identifier>PMID: 26582554</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Animals ; Biomedical and Life Sciences ; Biomedicine ; Cell Fusion ; Cellular biology ; Chlorocebus aethiops ; Epithelial Cells - virology ; HN Protein - genetics ; HN Protein - metabolism ; Immunology ; Influenza ; Influenza A virus ; Influenza A virus - growth & development ; Medical Microbiology ; Microbial Interactions ; Original Investigation ; Parainfluenza virus ; Parainfluenza Virus 2, Human - genetics ; Parainfluenza Virus 2, Human - growth & development ; Vero Cells ; Viral Fusion Proteins - genetics ; Viral Fusion Proteins - metabolism ; Viral infections ; Virology ; Virus Cultivation</subject><ispartof>Medical microbiology and immunology, 2016-06, Vol.205 (3), p.209-218</ispartof><rights>Springer-Verlag Berlin Heidelberg 2015</rights><rights>Springer-Verlag Berlin Heidelberg 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-875c096cbae2e6ca013a315ee3dc618d7f8f5a681b0d0ad70a562b9bdaadf7ca3</citedby><cites>FETCH-LOGICAL-c503t-875c096cbae2e6ca013a315ee3dc618d7f8f5a681b0d0ad70a562b9bdaadf7ca3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00430-015-0441-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00430-015-0441-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27903,27904,41467,42536,51298</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26582554$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Goto, Hideo</creatorcontrib><creatorcontrib>Ihira, Hironobu</creatorcontrib><creatorcontrib>Morishita, Keiichi</creatorcontrib><creatorcontrib>Tsuchiya, Mitsuki</creatorcontrib><creatorcontrib>Ohta, Keisuke</creatorcontrib><creatorcontrib>Yumine, Natsuko</creatorcontrib><creatorcontrib>Tsurudome, Masato</creatorcontrib><creatorcontrib>Nishio, Machiko</creatorcontrib><title>Enhanced growth of influenza A virus by coinfection with human parainfluenza virus type 2</title><title>Medical microbiology and immunology</title><addtitle>Med Microbiol Immunol</addtitle><addtitle>Med Microbiol Immunol</addtitle><description>It has been reported that dual or multiple viruses can coinfect epithelial cells of the respiratory tract. However, little has been reported on in vitro interactions of coinfected viruses. To explore how coinfection of different viruses affects their biological property, we examined growth of influenza A virus (IAV) and human parainfluenza virus type 2 (hPIV2) during coinfection of Vero cells. We found that IAV growth was enhanced by coinfection with hPIV2. The enhanced growth of IAV was not reproduced by coinfection with an hPIV2 mutant with reduced cell fusion activity, or by ectopic expression of the V protein of hPIV2. In contrast, induction of cell fusion by ectopic expression of the hPIV2 HN and F proteins augments IAV growth. hPIV2 coinfection supported IAV growth in cells originated from the respiratory epithelium. The enhancement correlated closely with cell fusion ability of hPIV2 in those cells. These results indicate that cell fusion induced by hPIV2 infection is beneficial to IAV replication and that enhanced viral replication by coinfection with different viruses can modify their pathological consequences.</description><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Fusion</subject><subject>Cellular biology</subject><subject>Chlorocebus aethiops</subject><subject>Epithelial Cells - virology</subject><subject>HN Protein - genetics</subject><subject>HN Protein - metabolism</subject><subject>Immunology</subject><subject>Influenza</subject><subject>Influenza A virus</subject><subject>Influenza A virus - growth & development</subject><subject>Medical Microbiology</subject><subject>Microbial Interactions</subject><subject>Original Investigation</subject><subject>Parainfluenza virus</subject><subject>Parainfluenza Virus 2, Human - genetics</subject><subject>Parainfluenza Virus 2, Human - growth & development</subject><subject>Vero Cells</subject><subject>Viral Fusion Proteins - 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virology</topic><topic>HN Protein - genetics</topic><topic>HN Protein - metabolism</topic><topic>Immunology</topic><topic>Influenza</topic><topic>Influenza A virus</topic><topic>Influenza A virus - growth & development</topic><topic>Medical Microbiology</topic><topic>Microbial Interactions</topic><topic>Original Investigation</topic><topic>Parainfluenza virus</topic><topic>Parainfluenza Virus 2, Human - genetics</topic><topic>Parainfluenza Virus 2, Human - growth & development</topic><topic>Vero Cells</topic><topic>Viral Fusion Proteins - genetics</topic><topic>Viral Fusion Proteins - metabolism</topic><topic>Viral infections</topic><topic>Virology</topic><topic>Virus Cultivation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Goto, Hideo</creatorcontrib><creatorcontrib>Ihira, Hironobu</creatorcontrib><creatorcontrib>Morishita, Keiichi</creatorcontrib><creatorcontrib>Tsuchiya, Mitsuki</creatorcontrib><creatorcontrib>Ohta, Keisuke</creatorcontrib><creatorcontrib>Yumine, Natsuko</creatorcontrib><creatorcontrib>Tsurudome, Masato</creatorcontrib><creatorcontrib>Nishio, Machiko</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Medical microbiology and immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Goto, Hideo</au><au>Ihira, Hironobu</au><au>Morishita, Keiichi</au><au>Tsuchiya, Mitsuki</au><au>Ohta, Keisuke</au><au>Yumine, Natsuko</au><au>Tsurudome, Masato</au><au>Nishio, Machiko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Enhanced growth of influenza A virus by coinfection with human parainfluenza virus type 2</atitle><jtitle>Medical microbiology and immunology</jtitle><stitle>Med Microbiol Immunol</stitle><addtitle>Med Microbiol Immunol</addtitle><date>2016-06-01</date><risdate>2016</risdate><volume>205</volume><issue>3</issue><spage>209</spage><epage>218</epage><pages>209-218</pages><issn>0300-8584</issn><eissn>1432-1831</eissn><abstract>It has been reported that dual or multiple viruses can coinfect epithelial cells of the respiratory tract. However, little has been reported on in vitro interactions of coinfected viruses. To explore how coinfection of different viruses affects their biological property, we examined growth of influenza A virus (IAV) and human parainfluenza virus type 2 (hPIV2) during coinfection of Vero cells. We found that IAV growth was enhanced by coinfection with hPIV2. The enhanced growth of IAV was not reproduced by coinfection with an hPIV2 mutant with reduced cell fusion activity, or by ectopic expression of the V protein of hPIV2. In contrast, induction of cell fusion by ectopic expression of the hPIV2 HN and F proteins augments IAV growth. hPIV2 coinfection supported IAV growth in cells originated from the respiratory epithelium. The enhancement correlated closely with cell fusion ability of hPIV2 in those cells. These results indicate that cell fusion induced by hPIV2 infection is beneficial to IAV replication and that enhanced viral replication by coinfection with different viruses can modify their pathological consequences.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>26582554</pmid><doi>10.1007/s00430-015-0441-y</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Biomedical and Life Sciences Biomedicine Cell Fusion Cellular biology Chlorocebus aethiops Epithelial Cells - virology HN Protein - genetics HN Protein - metabolism Immunology Influenza Influenza A virus Influenza A virus - growth & development Medical Microbiology Microbial Interactions Original Investigation Parainfluenza virus Parainfluenza Virus 2, Human - genetics Parainfluenza Virus 2, Human - growth & development Vero Cells Viral Fusion Proteins - genetics Viral Fusion Proteins - metabolism Viral infections Virology Virus Cultivation |
title | Enhanced growth of influenza A virus by coinfection with human parainfluenza virus type 2 |
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