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...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Microbial pathogenesis 1989-03, Vol.6 (3), p.219-226
Hauptverfasser: Lai, Alexander C.-K., Pogo, Beatriz G.-T.
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 226
container_issue 3
container_start_page 219
container_title Microbial pathogenesis
container_volume 6
creator Lai, Alexander C.-K.
Pogo, Beatriz G.-T.
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
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_79062698</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>0882401089900715</els_id><sourcerecordid>15221812</sourcerecordid><originalsourceid>FETCH-LOGICAL-c332t-ec43cc280328348c74d256481d037a01f98af3f93fd0bb9ac8b9468c083723873</originalsourceid><addsrcrecordid>eNqFkc2LFDEQxYO4rOPof6CQg4geWitJfySXhWXxY2HBi55DprqyG-1Jj0m6Zf97e3aG8eaeiuL96lG8x9grAR8EiPYjaC2rGgS80-a9AehE1TxhKwGmrYQE_ZStTsgz9jznnwBgamXO2bnslGlasWLTZSkUJ1eo5z0NVMIY-XYqLpbMR89nhxhicHwOacp8cPgrxFte7uifdJvGP-WOe4dlTNwlWpw8YQkz8RB5ot0Q0D04L-sc5vEFO_NuyPTyONfsx-dP36--VjffvlxfXd5UqJQsFWGtEKUGJbWqNXZ1L5u21qIH1TkQ3mjnlTfK97DZGId6Y-pWI2jVSaU7tWZvD767NP6eKBe7DRlpGFykccq2M9DK1uhHQdFIKbSQC1gfQExjzom83aWwdeneCrD7Wuw-c7vP3GpjH2qxzXL2-ug_bbbUn46OPSz6m6PuMrrBJxcx5BPWSQN6qW7NLg4YLaHNgZLNGCgi9SEtgdt-DP__4y9roal5</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>15221812</pqid></control><display><type>article</type><title>Attenuated deletion mutants of vaccinia virus lacking the vaccinia growth factor are defective in replication in vivo</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals Complete</source><creator>Lai, Alexander C.-K. ; Pogo, Beatriz G.-T.</creator><creatorcontrib>Lai, Alexander C.-K. ; Pogo, Beatriz G.-T.</creatorcontrib><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><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>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=7290894$$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>
fulltext fulltext
identifier ISSN: 0882-4010
ispartof Microbial pathogenesis, 1989-03, Vol.6 (3), p.219-226
issn 0882-4010
1096-1208
language eng
recordid cdi_proquest_miscellaneous_79062698
source MEDLINE; Elsevier ScienceDirect Journals Complete
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
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-17T15%3A15%3A02IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Attenuated%20deletion%20mutants%20of%20vaccinia%20virus%20lacking%20the%20vaccinia%20growth%20factor%20are%20defective%20in%20replication%20in%20vivo&rft.jtitle=Microbial%20pathogenesis&rft.au=Lai,%20Alexander%20C.-K.&rft.date=1989-03&rft.volume=6&rft.issue=3&rft.spage=219&rft.epage=226&rft.pages=219-226&rft.issn=0882-4010&rft.eissn=1096-1208&rft.coden=MIPAEV&rft_id=info:doi/10.1016/0882-4010(89)90071-5&rft_dat=%3Cproquest_cross%3E15221812%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=15221812&rft_id=info:pmid/2739561&rft_els_id=0882401089900715&rfr_iscdi=true