Attenuated deletion mutants of vaccinia virus lacking the vaccinia growth factor are defective in replication in vivo
Understanding the molecular basis of virulence in poxvirus is of great importance for the development of recombinant vaccines using vaccinia virus as a vector. We have previously described mutants of vaccinia virus with deletions ranging from 20 to 21 kb at the left terminus and with attenuated phen...
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Veröffentlicht in: | Microbial pathogenesis 1989-03, Vol.6 (3), p.219-226 |
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description | Understanding the molecular basis of virulence in poxvirus is of great importance for the development of recombinant vaccines using vaccinia virus as a vector. We have previously described mutants of vaccinia virus with deletions ranging from 20 to 21 kb at the left terminus and with attenuated phenotype. The virulence of these mutants was studied, using different routes of inoculation, for protection from wild-type challenge in mice and for replication
in vivo. Regardless of the route of inoculation, the LD
50 of the deletion mutants is at least 1000-fold higher than that of the wild-type. Results from protection experiments using viable and ultraviolet-inactivated viruses, and from determination of infectivity in different organs, indicated that the mutants were unable to replicate
in vivo. Southern blot hybridization of viral DNA with pSC16, a plasmid containing the vaccinia growth factor (VGF) gene, revealed that in the IHD-W strain of vaccinia virus this gene is localized at the left terminus exclusively and that the mutants lack this gene. The results suggest that absence of the VGF gene is correlated with inability to replicate
in vivo and decreased virulence. |
doi_str_mv | 10.1016/0882-4010(89)90071-5 |
format | Article |
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in vivo. Regardless of the route of inoculation, the LD
50 of the deletion mutants is at least 1000-fold higher than that of the wild-type. Results from protection experiments using viable and ultraviolet-inactivated viruses, and from determination of infectivity in different organs, indicated that the mutants were unable to replicate
in vivo. Southern blot hybridization of viral DNA with pSC16, a plasmid containing the vaccinia growth factor (VGF) gene, revealed that in the IHD-W strain of vaccinia virus this gene is localized at the left terminus exclusively and that the mutants lack this gene. The results suggest that absence of the VGF gene is correlated with inability to replicate
in vivo and decreased virulence.</description><identifier>ISSN: 0882-4010</identifier><identifier>EISSN: 1096-1208</identifier><identifier>DOI: 10.1016/0882-4010(89)90071-5</identifier><identifier>PMID: 2739561</identifier><identifier>CODEN: MIPAEV</identifier><language>eng</language><publisher>Oxford: Elsevier India Pvt Ltd</publisher><subject>Animals ; Biological and medical sciences ; Blotting, Southern ; DNA, Viral - analysis ; Female ; Fundamental and applied biological sciences. Psychology ; growth factor ; Growth Substances - genetics ; Liver - microbiology ; Mice ; Microbiology ; Mutation ; Nucleic Acid Hybridization ; Peptides - genetics ; Phenotype ; protective immunity ; replication in vivo ; Spleen - microbiology ; Vaccines, antisera, therapeutical immunoglobulins and monoclonal antibodies ; Vaccinia - microbiology ; vaccinia virus ; Vaccinia virus - genetics ; Vaccinia virus - pathogenicity ; Vaccinia virus - physiology ; Virology ; Virulence ; Virus Replication</subject><ispartof>Microbial pathogenesis, 1989-03, Vol.6 (3), p.219-226</ispartof><rights>1989</rights><rights>1989 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c332t-ec43cc280328348c74d256481d037a01f98af3f93fd0bb9ac8b9468c083723873</citedby><cites>FETCH-LOGICAL-c332t-ec43cc280328348c74d256481d037a01f98af3f93fd0bb9ac8b9468c083723873</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0882-4010(89)90071-5$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7290894$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2739561$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lai, Alexander C.-K.</creatorcontrib><creatorcontrib>Pogo, Beatriz G.-T.</creatorcontrib><title>Attenuated deletion mutants of vaccinia virus lacking the vaccinia growth factor are defective in replication in vivo</title><title>Microbial pathogenesis</title><addtitle>Microb Pathog</addtitle><description>Understanding the molecular basis of virulence in poxvirus is of great importance for the development of recombinant vaccines using vaccinia virus as a vector. We have previously described mutants of vaccinia virus with deletions ranging from 20 to 21 kb at the left terminus and with attenuated phenotype. The virulence of these mutants was studied, using different routes of inoculation, for protection from wild-type challenge in mice and for replication
in vivo. Regardless of the route of inoculation, the LD
50 of the deletion mutants is at least 1000-fold higher than that of the wild-type. Results from protection experiments using viable and ultraviolet-inactivated viruses, and from determination of infectivity in different organs, indicated that the mutants were unable to replicate
in vivo. Southern blot hybridization of viral DNA with pSC16, a plasmid containing the vaccinia growth factor (VGF) gene, revealed that in the IHD-W strain of vaccinia virus this gene is localized at the left terminus exclusively and that the mutants lack this gene. The results suggest that absence of the VGF gene is correlated with inability to replicate
in vivo and decreased virulence.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blotting, Southern</subject><subject>DNA, Viral - analysis</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>growth factor</subject><subject>Growth Substances - genetics</subject><subject>Liver - microbiology</subject><subject>Mice</subject><subject>Microbiology</subject><subject>Mutation</subject><subject>Nucleic Acid Hybridization</subject><subject>Peptides - genetics</subject><subject>Phenotype</subject><subject>protective immunity</subject><subject>replication in vivo</subject><subject>Spleen - microbiology</subject><subject>Vaccines, antisera, therapeutical immunoglobulins and monoclonal antibodies</subject><subject>Vaccinia - microbiology</subject><subject>vaccinia virus</subject><subject>Vaccinia virus - genetics</subject><subject>Vaccinia virus - pathogenicity</subject><subject>Vaccinia virus - physiology</subject><subject>Virology</subject><subject>Virulence</subject><subject>Virus Replication</subject><issn>0882-4010</issn><issn>1096-1208</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1989</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc2LFDEQxYO4rOPof6CQg4geWitJfySXhWXxY2HBi55DprqyG-1Jj0m6Zf97e3aG8eaeiuL96lG8x9grAR8EiPYjaC2rGgS80-a9AehE1TxhKwGmrYQE_ZStTsgz9jznnwBgamXO2bnslGlasWLTZSkUJ1eo5z0NVMIY-XYqLpbMR89nhxhicHwOacp8cPgrxFte7uifdJvGP-WOe4dlTNwlWpw8YQkz8RB5ot0Q0D04L-sc5vEFO_NuyPTyONfsx-dP36--VjffvlxfXd5UqJQsFWGtEKUGJbWqNXZ1L5u21qIH1TkQ3mjnlTfK97DZGId6Y-pWI2jVSaU7tWZvD767NP6eKBe7DRlpGFykccq2M9DK1uhHQdFIKbSQC1gfQExjzom83aWwdeneCrD7Wuw-c7vP3GpjH2qxzXL2-ug_bbbUn46OPSz6m6PuMrrBJxcx5BPWSQN6qW7NLg4YLaHNgZLNGCgi9SEtgdt-DP__4y9roal5</recordid><startdate>198903</startdate><enddate>198903</enddate><creator>Lai, Alexander C.-K.</creator><creator>Pogo, Beatriz G.-T.</creator><general>Elsevier India Pvt Ltd</general><general>Elsevier</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>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>198903</creationdate><title>Attenuated deletion mutants of vaccinia virus lacking the vaccinia growth factor are defective in replication in vivo</title><author>Lai, Alexander C.-K. ; Pogo, Beatriz G.-T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c332t-ec43cc280328348c74d256481d037a01f98af3f93fd0bb9ac8b9468c083723873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1989</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blotting, Southern</topic><topic>DNA, Viral - analysis</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>growth factor</topic><topic>Growth Substances - genetics</topic><topic>Liver - microbiology</topic><topic>Mice</topic><topic>Microbiology</topic><topic>Mutation</topic><topic>Nucleic Acid Hybridization</topic><topic>Peptides - genetics</topic><topic>Phenotype</topic><topic>protective immunity</topic><topic>replication in vivo</topic><topic>Spleen - microbiology</topic><topic>Vaccines, antisera, therapeutical immunoglobulins and monoclonal antibodies</topic><topic>Vaccinia - microbiology</topic><topic>vaccinia virus</topic><topic>Vaccinia virus - genetics</topic><topic>Vaccinia virus - pathogenicity</topic><topic>Vaccinia virus - physiology</topic><topic>Virology</topic><topic>Virulence</topic><topic>Virus Replication</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lai, Alexander C.-K.</creatorcontrib><creatorcontrib>Pogo, Beatriz G.-T.</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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Microbial pathogenesis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lai, Alexander C.-K.</au><au>Pogo, Beatriz G.-T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Attenuated deletion mutants of vaccinia virus lacking the vaccinia growth factor are defective in replication in vivo</atitle><jtitle>Microbial pathogenesis</jtitle><addtitle>Microb Pathog</addtitle><date>1989-03</date><risdate>1989</risdate><volume>6</volume><issue>3</issue><spage>219</spage><epage>226</epage><pages>219-226</pages><issn>0882-4010</issn><eissn>1096-1208</eissn><coden>MIPAEV</coden><abstract>Understanding the molecular basis of virulence in poxvirus is of great importance for the development of recombinant vaccines using vaccinia virus as a vector. We have previously described mutants of vaccinia virus with deletions ranging from 20 to 21 kb at the left terminus and with attenuated phenotype. The virulence of these mutants was studied, using different routes of inoculation, for protection from wild-type challenge in mice and for replication
in vivo. Regardless of the route of inoculation, the LD
50 of the deletion mutants is at least 1000-fold higher than that of the wild-type. Results from protection experiments using viable and ultraviolet-inactivated viruses, and from determination of infectivity in different organs, indicated that the mutants were unable to replicate
in vivo. Southern blot hybridization of viral DNA with pSC16, a plasmid containing the vaccinia growth factor (VGF) gene, revealed that in the IHD-W strain of vaccinia virus this gene is localized at the left terminus exclusively and that the mutants lack this gene. The results suggest that absence of the VGF gene is correlated with inability to replicate
in vivo and decreased virulence.</abstract><cop>Oxford</cop><pub>Elsevier India Pvt Ltd</pub><pmid>2739561</pmid><doi>10.1016/0882-4010(89)90071-5</doi><tpages>8</tpages></addata></record> |
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subjects | Animals Biological and medical sciences Blotting, Southern DNA, Viral - analysis Female Fundamental and applied biological sciences. Psychology growth factor Growth Substances - genetics Liver - microbiology Mice Microbiology Mutation Nucleic Acid Hybridization Peptides - genetics Phenotype protective immunity replication in vivo Spleen - microbiology Vaccines, antisera, therapeutical immunoglobulins and monoclonal antibodies Vaccinia - microbiology vaccinia virus Vaccinia virus - genetics Vaccinia virus - pathogenicity Vaccinia virus - physiology Virology Virulence Virus Replication |
title | Attenuated deletion mutants of vaccinia virus lacking the vaccinia growth factor are defective in replication in vivo |
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