The molecular basis of mouse adaptation by human enterovirus 71
1 Division of Virology, Telethon Institute for Child Health Research, Perth, Australia 2 School of Veterinary and Biomedical Sciences, Murdoch University, Perth, Australia 3 Discipline of Infectious Diseases and Immunology, The University of Sydney, Australia Correspondence Peter C. McMinn pmcminn{a...
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| Veröffentlicht in: | Journal of general virology 2008-07, Vol.89 (7), p.1622-1632 |
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| creator | Chua, Beng Hooi Phuektes, Patchara Sanders, Sharon A Nicholls, Philip K McMinn, Peter C |
| description | 1 Division of Virology, Telethon Institute for Child Health Research, Perth, Australia
2 School of Veterinary and Biomedical Sciences, Murdoch University, Perth, Australia
3 Discipline of Infectious Diseases and Immunology, The University of Sydney, Australia
Correspondence Peter C. McMinn pmcminn{at}med.usyd.edu.au
A mouse-adapted strain of human enterovirus 71 (HEV71) was selected by serial passage of a HEV71 clinical isolate (HEV71-26M) in Chinese hamster ovary (CHO) cells (CHO-26M) and in newborn BALB/c mice (MP-26M). Despite improved growth in CHO cells, CHO-26M did not show increased virulence in newborn BALB/c mice compared with HEV71-26M. By contrast, infection of newborn mice with MP-26M resulted in severe disease of high mortality. Skeletal muscle was the primary site of replication in mice for both viruses. However, MP-26M infection induced severe necrotizing myositis, whereas CHO-26M infection caused only mild inflammation. MP-26M was also isolated from whole blood, heart, liver, spleen and brain of infected mice. CHO-26M harboured a single mutation within the open reading frame (ORF), resulting in an amino acid substitution of K 149 I in the VP2 capsid protein; two further ORF mutations that resulted in amino acid substitutions were identified in MP-26M, located within the VP1 capsid protein (G 145 E) and the 2C protein (K 216 R). Infectious cDNA clone-derived mutant virus populations containing the mutations identified in CHO-26M and MP-26M were generated in order to study the molecular basis of CHO cell and mouse adaptation. The VP2 (K 149 I) change was responsible only for improved growth in CHO cells and did not lead to increased virulence in mice. Of the two amino acid substitutions identified in MP-26M, the VP1 (G 145 E) mutation alone was sufficient to increase virulence in mice to the level observed in MP-26M-infected mice.
These authors contributed equally to this work.
The GenBank/EMBL/DDBJ accession numbers for the sequences reported in this paper are EU364841 (HEV71-26M), EU376004 (CHO-26M) and EU376005 (MP-26M). |
| doi_str_mv | 10.1099/vir.0.83676-0 |
| format | Article |
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2 School of Veterinary and Biomedical Sciences, Murdoch University, Perth, Australia
3 Discipline of Infectious Diseases and Immunology, The University of Sydney, Australia
Correspondence Peter C. McMinn pmcminn{at}med.usyd.edu.au
A mouse-adapted strain of human enterovirus 71 (HEV71) was selected by serial passage of a HEV71 clinical isolate (HEV71-26M) in Chinese hamster ovary (CHO) cells (CHO-26M) and in newborn BALB/c mice (MP-26M). Despite improved growth in CHO cells, CHO-26M did not show increased virulence in newborn BALB/c mice compared with HEV71-26M. By contrast, infection of newborn mice with MP-26M resulted in severe disease of high mortality. Skeletal muscle was the primary site of replication in mice for both viruses. However, MP-26M infection induced severe necrotizing myositis, whereas CHO-26M infection caused only mild inflammation. MP-26M was also isolated from whole blood, heart, liver, spleen and brain of infected mice. CHO-26M harboured a single mutation within the open reading frame (ORF), resulting in an amino acid substitution of K 149 I in the VP2 capsid protein; two further ORF mutations that resulted in amino acid substitutions were identified in MP-26M, located within the VP1 capsid protein (G 145 E) and the 2C protein (K 216 R). Infectious cDNA clone-derived mutant virus populations containing the mutations identified in CHO-26M and MP-26M were generated in order to study the molecular basis of CHO cell and mouse adaptation. The VP2 (K 149 I) change was responsible only for improved growth in CHO cells and did not lead to increased virulence in mice. Of the two amino acid substitutions identified in MP-26M, the VP1 (G 145 E) mutation alone was sufficient to increase virulence in mice to the level observed in MP-26M-infected mice.
These authors contributed equally to this work.
The GenBank/EMBL/DDBJ accession numbers for the sequences reported in this paper are EU364841 (HEV71-26M), EU376004 (CHO-26M) and EU376005 (MP-26M).</description><identifier>ISSN: 0022-1317</identifier><identifier>EISSN: 1465-2099</identifier><identifier>DOI: 10.1099/vir.0.83676-0</identifier><identifier>PMID: 18559932</identifier><identifier>CODEN: JGVIAY</identifier><language>eng</language><publisher>Reading: Soc General Microbiol</publisher><subject>Adaptation, Biological ; Amino Acid Substitution - genetics ; Animals ; Animals, Newborn ; Biological and medical sciences ; CHO Cells ; Cricetinae ; Cricetulus ; DNA Mutational Analysis ; Enterovirus A, Human - genetics ; Enterovirus A, Human - growth & development ; Enterovirus A, Human - pathogenicity ; Enterovirus Infections - virology ; Fundamental and applied biological sciences. Psychology ; Host-Pathogen Interactions ; Human enterovirus 71 ; Humans ; Mice ; Mice, Inbred BALB C ; Microbiology ; Miscellaneous ; Molecular Sequence Data ; Muscle, Skeletal - pathology ; Muscle, Skeletal - virology ; Mutation, Missense ; Myositis - virology ; Necrosis ; Sequence Analysis, DNA ; Serial Passage ; Survival Analysis ; Viral Structural Proteins - genetics ; Virology ; Virulence</subject><ispartof>Journal of general virology, 2008-07, Vol.89 (7), p.1622-1632</ispartof><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-a95778fb538a9102158048f8a38dd3ed3378eeb7cba4bcc5a666b5c4dfa529313</citedby><cites>FETCH-LOGICAL-c490t-a95778fb538a9102158048f8a38dd3ed3378eeb7cba4bcc5a666b5c4dfa529313</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,3747,3748,27926,27927</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20478757$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18559932$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chua, Beng Hooi</creatorcontrib><creatorcontrib>Phuektes, Patchara</creatorcontrib><creatorcontrib>Sanders, Sharon A</creatorcontrib><creatorcontrib>Nicholls, Philip K</creatorcontrib><creatorcontrib>McMinn, Peter C</creatorcontrib><title>The molecular basis of mouse adaptation by human enterovirus 71</title><title>Journal of general virology</title><addtitle>J Gen Virol</addtitle><description>1 Division of Virology, Telethon Institute for Child Health Research, Perth, Australia
2 School of Veterinary and Biomedical Sciences, Murdoch University, Perth, Australia
3 Discipline of Infectious Diseases and Immunology, The University of Sydney, Australia
Correspondence Peter C. McMinn pmcminn{at}med.usyd.edu.au
A mouse-adapted strain of human enterovirus 71 (HEV71) was selected by serial passage of a HEV71 clinical isolate (HEV71-26M) in Chinese hamster ovary (CHO) cells (CHO-26M) and in newborn BALB/c mice (MP-26M). Despite improved growth in CHO cells, CHO-26M did not show increased virulence in newborn BALB/c mice compared with HEV71-26M. By contrast, infection of newborn mice with MP-26M resulted in severe disease of high mortality. Skeletal muscle was the primary site of replication in mice for both viruses. However, MP-26M infection induced severe necrotizing myositis, whereas CHO-26M infection caused only mild inflammation. MP-26M was also isolated from whole blood, heart, liver, spleen and brain of infected mice. CHO-26M harboured a single mutation within the open reading frame (ORF), resulting in an amino acid substitution of K 149 I in the VP2 capsid protein; two further ORF mutations that resulted in amino acid substitutions were identified in MP-26M, located within the VP1 capsid protein (G 145 E) and the 2C protein (K 216 R). Infectious cDNA clone-derived mutant virus populations containing the mutations identified in CHO-26M and MP-26M were generated in order to study the molecular basis of CHO cell and mouse adaptation. The VP2 (K 149 I) change was responsible only for improved growth in CHO cells and did not lead to increased virulence in mice. Of the two amino acid substitutions identified in MP-26M, the VP1 (G 145 E) mutation alone was sufficient to increase virulence in mice to the level observed in MP-26M-infected mice.
These authors contributed equally to this work.
The GenBank/EMBL/DDBJ accession numbers for the sequences reported in this paper are EU364841 (HEV71-26M), EU376004 (CHO-26M) and EU376005 (MP-26M).</description><subject>Adaptation, Biological</subject><subject>Amino Acid Substitution - genetics</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Biological and medical sciences</subject><subject>CHO Cells</subject><subject>Cricetinae</subject><subject>Cricetulus</subject><subject>DNA Mutational Analysis</subject><subject>Enterovirus A, Human - genetics</subject><subject>Enterovirus A, Human - growth & development</subject><subject>Enterovirus A, Human - pathogenicity</subject><subject>Enterovirus Infections - virology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Host-Pathogen Interactions</subject><subject>Human enterovirus 71</subject><subject>Humans</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Microbiology</subject><subject>Miscellaneous</subject><subject>Molecular Sequence Data</subject><subject>Muscle, Skeletal - pathology</subject><subject>Muscle, Skeletal - virology</subject><subject>Mutation, Missense</subject><subject>Myositis - virology</subject><subject>Necrosis</subject><subject>Sequence Analysis, DNA</subject><subject>Serial Passage</subject><subject>Survival Analysis</subject><subject>Viral Structural Proteins - genetics</subject><subject>Virology</subject><subject>Virulence</subject><issn>0022-1317</issn><issn>1465-2099</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpF0ElLBDEQBeAgio7L0av0RfHSY9ZOchIRNxC8jOdQSaedSC9j0q347804g54ClY-qx0PolOA5wVpffYY4x3PFKlmVeAfNCK9ESfPPLpphTGlJGJEH6DCld4wJ50LuowOihNCa0Rm6Xix90Q2td1MLsbCQQiqGJo-m5AuoYTXCGIa-sN_FcuqgL3w_-jjks1MqJDlGew20yZ9s3yP0en-3uH0sn18enm5vnkvHNR5L0EJK1VjBFGiCKREKc9UoYKquma8Zk8p7K50Fbp0TUFWVFY7XDQiqGWFH6GKzdxWHj8mn0XQhOd-20Psc1RBdYa45zbDcQBeHlKJvzCqGDuK3IdisGzM5usHmtzGDsz_bLp5s5-t_va0og_MtgOSgbSL0LqQ_RzGXSgqZ3eXGLcPb8itEb95834Ucw4ZhfVRpIw2pKGU_iDOBrg</recordid><startdate>20080701</startdate><enddate>20080701</enddate><creator>Chua, Beng Hooi</creator><creator>Phuektes, Patchara</creator><creator>Sanders, Sharon A</creator><creator>Nicholls, Philip K</creator><creator>McMinn, Peter C</creator><general>Soc General Microbiol</general><general>Society for General Microbiology</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U9</scope><scope>H94</scope></search><sort><creationdate>20080701</creationdate><title>The molecular basis of mouse adaptation by human enterovirus 71</title><author>Chua, Beng Hooi ; Phuektes, Patchara ; Sanders, Sharon A ; Nicholls, Philip K ; McMinn, Peter C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c490t-a95778fb538a9102158048f8a38dd3ed3378eeb7cba4bcc5a666b5c4dfa529313</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adaptation, Biological</topic><topic>Amino Acid Substitution - genetics</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Biological and medical sciences</topic><topic>CHO Cells</topic><topic>Cricetinae</topic><topic>Cricetulus</topic><topic>DNA Mutational Analysis</topic><topic>Enterovirus A, Human - genetics</topic><topic>Enterovirus A, Human - growth & development</topic><topic>Enterovirus A, Human - pathogenicity</topic><topic>Enterovirus Infections - virology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Host-Pathogen Interactions</topic><topic>Human enterovirus 71</topic><topic>Humans</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Microbiology</topic><topic>Miscellaneous</topic><topic>Molecular Sequence Data</topic><topic>Muscle, Skeletal - pathology</topic><topic>Muscle, Skeletal - virology</topic><topic>Mutation, Missense</topic><topic>Myositis - virology</topic><topic>Necrosis</topic><topic>Sequence Analysis, DNA</topic><topic>Serial Passage</topic><topic>Survival Analysis</topic><topic>Viral Structural Proteins - genetics</topic><topic>Virology</topic><topic>Virulence</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chua, Beng Hooi</creatorcontrib><creatorcontrib>Phuektes, Patchara</creatorcontrib><creatorcontrib>Sanders, Sharon A</creatorcontrib><creatorcontrib>Nicholls, Philip K</creatorcontrib><creatorcontrib>McMinn, Peter C</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Journal of general virology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chua, Beng Hooi</au><au>Phuektes, Patchara</au><au>Sanders, Sharon A</au><au>Nicholls, Philip K</au><au>McMinn, Peter C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The molecular basis of mouse adaptation by human enterovirus 71</atitle><jtitle>Journal of general virology</jtitle><addtitle>J Gen Virol</addtitle><date>2008-07-01</date><risdate>2008</risdate><volume>89</volume><issue>7</issue><spage>1622</spage><epage>1632</epage><pages>1622-1632</pages><issn>0022-1317</issn><eissn>1465-2099</eissn><coden>JGVIAY</coden><abstract>1 Division of Virology, Telethon Institute for Child Health Research, Perth, Australia
2 School of Veterinary and Biomedical Sciences, Murdoch University, Perth, Australia
3 Discipline of Infectious Diseases and Immunology, The University of Sydney, Australia
Correspondence Peter C. McMinn pmcminn{at}med.usyd.edu.au
A mouse-adapted strain of human enterovirus 71 (HEV71) was selected by serial passage of a HEV71 clinical isolate (HEV71-26M) in Chinese hamster ovary (CHO) cells (CHO-26M) and in newborn BALB/c mice (MP-26M). Despite improved growth in CHO cells, CHO-26M did not show increased virulence in newborn BALB/c mice compared with HEV71-26M. By contrast, infection of newborn mice with MP-26M resulted in severe disease of high mortality. Skeletal muscle was the primary site of replication in mice for both viruses. However, MP-26M infection induced severe necrotizing myositis, whereas CHO-26M infection caused only mild inflammation. MP-26M was also isolated from whole blood, heart, liver, spleen and brain of infected mice. CHO-26M harboured a single mutation within the open reading frame (ORF), resulting in an amino acid substitution of K 149 I in the VP2 capsid protein; two further ORF mutations that resulted in amino acid substitutions were identified in MP-26M, located within the VP1 capsid protein (G 145 E) and the 2C protein (K 216 R). Infectious cDNA clone-derived mutant virus populations containing the mutations identified in CHO-26M and MP-26M were generated in order to study the molecular basis of CHO cell and mouse adaptation. The VP2 (K 149 I) change was responsible only for improved growth in CHO cells and did not lead to increased virulence in mice. Of the two amino acid substitutions identified in MP-26M, the VP1 (G 145 E) mutation alone was sufficient to increase virulence in mice to the level observed in MP-26M-infected mice.
These authors contributed equally to this work.
The GenBank/EMBL/DDBJ accession numbers for the sequences reported in this paper are EU364841 (HEV71-26M), EU376004 (CHO-26M) and EU376005 (MP-26M).</abstract><cop>Reading</cop><pub>Soc General Microbiol</pub><pmid>18559932</pmid><doi>10.1099/vir.0.83676-0</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptation, Biological Amino Acid Substitution - genetics Animals Animals, Newborn Biological and medical sciences CHO Cells Cricetinae Cricetulus DNA Mutational Analysis Enterovirus A, Human - genetics Enterovirus A, Human - growth & development Enterovirus A, Human - pathogenicity Enterovirus Infections - virology Fundamental and applied biological sciences. Psychology Host-Pathogen Interactions Human enterovirus 71 Humans Mice Mice, Inbred BALB C Microbiology Miscellaneous Molecular Sequence Data Muscle, Skeletal - pathology Muscle, Skeletal - virology Mutation, Missense Myositis - virology Necrosis Sequence Analysis, DNA Serial Passage Survival Analysis Viral Structural Proteins - genetics Virology Virulence |
| title | The molecular basis of mouse adaptation by human enterovirus 71 |
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