Up-regulation of Murid herpesvirus 4 ORF50 by hypoxia: Possible implication for virus reactivation from latency
Murid herpesvirus 4 (MuHV-4) is a member of the Gammaherpesvirus subfamily capable to establish a long-lasting latency and induce occasional malignancies. Because MuHV-4 is associated with cancer in a subset of virus-infected mice and because tumor development is often linked with hypoxia, we studie...
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| Veröffentlicht in: | Virus research 2008-03, Vol.132 (1), p.257-262 |
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| creator | Polcicova, Katarina Hrabovska, Zuzana Mistrikova, Jela Tomaskova, Jana Pastorek, Jaromir Pastorekova, Silvia Kopacek, Juraj |
| description | Murid herpesvirus 4 (MuHV-4) is a member of the Gammaherpesvirus subfamily capable to establish a long-lasting latency and induce occasional malignancies. Because MuHV-4 is associated with cancer in a subset of virus-infected mice and because tumor development is often linked with hypoxia, we studied the influence of hypoxia on the biology of this virus. Using immunofluorescence and FACS analysis we detected increased proportion of MuHV-4 positive cells in the latently infected NB-78 cell line exposed to low oxygen conditions compared to normoxic controls. Moreover, the expression of ORF50, a crucial gene responsible for switch from latency to lytic virus replication, was induced upon the exposure of NB-78 cells to hypoxia. Luciferase reporter assays with ORF50 promoter confirmed the hypoxia-dependent induction. Transient co-transfections with hypoxia inducible factors showed that HIF-2α is a more potent activator of ORF50 expression than HIF-1α. Our results confirm that the MuHV-4 life cycle is influenced by low oxygen concentration. |
| doi_str_mv | 10.1016/j.virusres.2007.12.004 |
| format | Article |
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Because MuHV-4 is associated with cancer in a subset of virus-infected mice and because tumor development is often linked with hypoxia, we studied the influence of hypoxia on the biology of this virus. Using immunofluorescence and FACS analysis we detected increased proportion of MuHV-4 positive cells in the latently infected NB-78 cell line exposed to low oxygen conditions compared to normoxic controls. Moreover, the expression of ORF50, a crucial gene responsible for switch from latency to lytic virus replication, was induced upon the exposure of NB-78 cells to hypoxia. Luciferase reporter assays with ORF50 promoter confirmed the hypoxia-dependent induction. Transient co-transfections with hypoxia inducible factors showed that HIF-2α is a more potent activator of ORF50 expression than HIF-1α. Our results confirm that the MuHV-4 life cycle is influenced by low oxygen concentration.</description><identifier>ISSN: 0168-1702</identifier><identifier>EISSN: 1872-7492</identifier><identifier>DOI: 10.1016/j.virusres.2007.12.004</identifier><identifier>PMID: 18221814</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Antigens, Viral - metabolism ; Basic Helix-Loop-Helix Transcription Factors - metabolism ; Cell Hypoxia ; Cell Line, Tumor ; Gammaherpesvirus ; Gene Expression Regulation, Viral ; Genes, Reporter ; Humans ; Hypoxia ; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism ; Latent infection ; Mice ; Murid herpesvirus 4 ; Open Reading Frames ; ORF50 ; Oxygen - metabolism ; Oxygen - pharmacology ; Promoter Regions, Genetic ; Rhadinovirus - genetics ; Rhadinovirus - physiology ; Time Factors ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Up-Regulation ; Virus Activation ; Virus Latency</subject><ispartof>Virus research, 2008-03, Vol.132 (1), p.257-262</ispartof><rights>2007 Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c397t-22dd6d4c8d34d7bb699226c632db614921bf7befcfea2b4db5a13c2c7c51390b3</citedby><cites>FETCH-LOGICAL-c397t-22dd6d4c8d34d7bb699226c632db614921bf7befcfea2b4db5a13c2c7c51390b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.virusres.2007.12.004$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18221814$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Polcicova, Katarina</creatorcontrib><creatorcontrib>Hrabovska, Zuzana</creatorcontrib><creatorcontrib>Mistrikova, Jela</creatorcontrib><creatorcontrib>Tomaskova, Jana</creatorcontrib><creatorcontrib>Pastorek, Jaromir</creatorcontrib><creatorcontrib>Pastorekova, Silvia</creatorcontrib><creatorcontrib>Kopacek, Juraj</creatorcontrib><title>Up-regulation of Murid herpesvirus 4 ORF50 by hypoxia: Possible implication for virus reactivation from latency</title><title>Virus research</title><addtitle>Virus Res</addtitle><description>Murid herpesvirus 4 (MuHV-4) is a member of the Gammaherpesvirus subfamily capable to establish a long-lasting latency and induce occasional malignancies. Because MuHV-4 is associated with cancer in a subset of virus-infected mice and because tumor development is often linked with hypoxia, we studied the influence of hypoxia on the biology of this virus. Using immunofluorescence and FACS analysis we detected increased proportion of MuHV-4 positive cells in the latently infected NB-78 cell line exposed to low oxygen conditions compared to normoxic controls. Moreover, the expression of ORF50, a crucial gene responsible for switch from latency to lytic virus replication, was induced upon the exposure of NB-78 cells to hypoxia. Luciferase reporter assays with ORF50 promoter confirmed the hypoxia-dependent induction. Transient co-transfections with hypoxia inducible factors showed that HIF-2α is a more potent activator of ORF50 expression than HIF-1α. Our results confirm that the MuHV-4 life cycle is influenced by low oxygen concentration.</description><subject>Animals</subject><subject>Antigens, Viral - metabolism</subject><subject>Basic Helix-Loop-Helix Transcription Factors - metabolism</subject><subject>Cell Hypoxia</subject><subject>Cell Line, Tumor</subject><subject>Gammaherpesvirus</subject><subject>Gene Expression Regulation, Viral</subject><subject>Genes, Reporter</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</subject><subject>Latent infection</subject><subject>Mice</subject><subject>Murid herpesvirus 4</subject><subject>Open Reading Frames</subject><subject>ORF50</subject><subject>Oxygen - metabolism</subject><subject>Oxygen - pharmacology</subject><subject>Promoter Regions, Genetic</subject><subject>Rhadinovirus - genetics</subject><subject>Rhadinovirus - physiology</subject><subject>Time Factors</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Up-Regulation</subject><subject>Virus Activation</subject><subject>Virus Latency</subject><issn>0168-1702</issn><issn>1872-7492</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcFO3DAQhq2Kqiy0r4B84pZ07HjthBMIAUWioqrK2YrtSfEqWQc7WbFvX9Ns1SMnS9b3z6-Zj5AzBiUDJr9uyp2Pc4qYSg6gSsZLAPGBrFiteKFEw4_IKoN1wRTwY3KS0gYAZKXkJ3LMas5ZzcSKhKexiPh77tvJhy0NHf0-R-_oM8YR098OKujjz9s1ULOnz_sxvPr2gv4IKXnTI_XD2Hu7pLsQ6RKJ2NrJ7w7fMQw0F-DW7j-Tj13bJ_xyeE_J0-3Nr-tvxcPj3f311UNhq0ZNBefOSSds7SrhlDGyaTiXVlbcGcnydsx0ymBnO2y5Ec6sW1ZZbpVds6oBU52S82XuGMPLjGnSg08W-77dYpiTVlCBAKHeBTmshWgalkG5gDbm3SN2eox-aONeM9BvTvRG_3Oi35xoxnV2koNnh4bZDOj-xw4SMnC5AJgPsvMYdbI-Hwudj2gn7YJ_r-MPr4ujDA</recordid><startdate>20080301</startdate><enddate>20080301</enddate><creator>Polcicova, Katarina</creator><creator>Hrabovska, Zuzana</creator><creator>Mistrikova, Jela</creator><creator>Tomaskova, Jana</creator><creator>Pastorek, Jaromir</creator><creator>Pastorekova, Silvia</creator><creator>Kopacek, Juraj</creator><general>Elsevier B.V</general><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><scope>7X8</scope></search><sort><creationdate>20080301</creationdate><title>Up-regulation of Murid herpesvirus 4 ORF50 by hypoxia: Possible implication for virus reactivation from latency</title><author>Polcicova, Katarina ; 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Because MuHV-4 is associated with cancer in a subset of virus-infected mice and because tumor development is often linked with hypoxia, we studied the influence of hypoxia on the biology of this virus. Using immunofluorescence and FACS analysis we detected increased proportion of MuHV-4 positive cells in the latently infected NB-78 cell line exposed to low oxygen conditions compared to normoxic controls. Moreover, the expression of ORF50, a crucial gene responsible for switch from latency to lytic virus replication, was induced upon the exposure of NB-78 cells to hypoxia. Luciferase reporter assays with ORF50 promoter confirmed the hypoxia-dependent induction. Transient co-transfections with hypoxia inducible factors showed that HIF-2α is a more potent activator of ORF50 expression than HIF-1α. 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| ispartof | Virus research, 2008-03, Vol.132 (1), p.257-262 |
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| subjects | Animals Antigens, Viral - metabolism Basic Helix-Loop-Helix Transcription Factors - metabolism Cell Hypoxia Cell Line, Tumor Gammaherpesvirus Gene Expression Regulation, Viral Genes, Reporter Humans Hypoxia Hypoxia-Inducible Factor 1, alpha Subunit - metabolism Latent infection Mice Murid herpesvirus 4 Open Reading Frames ORF50 Oxygen - metabolism Oxygen - pharmacology Promoter Regions, Genetic Rhadinovirus - genetics Rhadinovirus - physiology Time Factors Transcription Factors - genetics Transcription Factors - metabolism Up-Regulation Virus Activation Virus Latency |
| title | Up-regulation of Murid herpesvirus 4 ORF50 by hypoxia: Possible implication for virus reactivation from latency |
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