Host-specific response to HCV infection in the chimeric SCID-beige/Alb-uPA mouse model: role of the innate antiviral immune response
The severe combined immunodeficiency disorder (SCID)-beige/albumin (Alb)-urokinase plasminogen activator (uPA) mouse containing a human-mouse chimeric liver is currently the only small animal model capable of supporting hepatitis C virus (HCV) infection. This model was utilized to characterize the h...
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| Veröffentlicht in: | PLoS pathogens 2006-06, Vol.2 (6), p.e59-e59 |
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| creator | Walters, Kathie-Anne Joyce, Michael A Thompson, Jill C Smith, Maria W Yeh, Matthew M Proll, Sean Zhu, Lin-Fu Gao, T J Kneteman, Norman M Tyrrell, D Lorne Katze, Michael G |
| description | The severe combined immunodeficiency disorder (SCID)-beige/albumin (Alb)-urokinase plasminogen activator (uPA) mouse containing a human-mouse chimeric liver is currently the only small animal model capable of supporting hepatitis C virus (HCV) infection. This model was utilized to characterize the host transcriptional response to HCV infection. The purpose of these studies was to investigate the genetic component of the host response to HCV infection and also to distinguish virus-induced gene expression changes from adaptive HCV-specific immune-mediated effects. Gene expression profiles from HCV-infected mice were also compared to those from HCV-infected patients. Analyses of the gene expression data demonstrate that host factors regulate the response to HCV infection, including the nature of the innate antiviral immune response. They also indicate that HCV mediates gene expression changes, including regulation of lipid metabolism genes, which have the potential to be directly cytopathic, indicating that liver pathology may not be exclusively mediated by HCV-specific adaptive immune responses. This effect appears to be inversely related to the activation of the innate antiviral immune response. In summary, the nature of the initial interferon response to HCV infection may determine the extent of viral-mediated effects on host gene expression. |
| doi_str_mv | 10.1371/journal.ppat.0020059 |
| format | Article |
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This model was utilized to characterize the host transcriptional response to HCV infection. The purpose of these studies was to investigate the genetic component of the host response to HCV infection and also to distinguish virus-induced gene expression changes from adaptive HCV-specific immune-mediated effects. Gene expression profiles from HCV-infected mice were also compared to those from HCV-infected patients. Analyses of the gene expression data demonstrate that host factors regulate the response to HCV infection, including the nature of the innate antiviral immune response. They also indicate that HCV mediates gene expression changes, including regulation of lipid metabolism genes, which have the potential to be directly cytopathic, indicating that liver pathology may not be exclusively mediated by HCV-specific adaptive immune responses. This effect appears to be inversely related to the activation of the innate antiviral immune response. In summary, the nature of the initial interferon response to HCV infection may determine the extent of viral-mediated effects on host gene expression.</description><identifier>ISSN: 1553-7374</identifier><identifier>ISSN: 1553-7366</identifier><identifier>EISSN: 1553-7374</identifier><identifier>DOI: 10.1371/journal.ppat.0020059</identifier><identifier>PMID: 16789836</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Albumins ; Animal models ; Animals ; Antibodies, Viral - biosynthesis ; Bioinformatics - Computational Biology ; Chimera ; Gastroenterology - Hepatology ; Gene expression ; Gene Expression Profiling ; Genetic aspects ; Hepatitis ; Hepatitis C ; Hepatitis C - genetics ; Hepatitis C - immunology ; Hepatitis C - metabolism ; Hepatocytes - transplantation ; Host-virus relationships ; Humans ; Immune response ; Immunity, Innate ; Infections ; Lipid Metabolism ; Liver - metabolism ; Medical research ; Mice ; Mice, SCID - genetics ; Mice, SCID - immunology ; Mus (Mouse) ; Oxidative Stress ; Physiological aspects ; Proteins ; Rodents ; Signal Transduction - immunology ; Urokinase-Type Plasminogen Activator - genetics ; Virology ; Viruses</subject><ispartof>PLoS pathogens, 2006-06, Vol.2 (6), p.e59-e59</ispartof><rights>COPYRIGHT 2006 Public Library of Science</rights><rights>2006 Walters et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Walters K-A, Joyce MA, Thompson JC, Smith MW, Yeh MM, et al. (2006) Host-Specific Response to HCV Infection in the Chimeric SCID-beige/Alb-uPA Mouse Model: Role of the Innate Antiviral Immune Response. PLoS Pathog 2(6): e59. doi:10.1371/journal.ppat.0020059</rights><rights>2006 Walters et al. 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c795t-ffd9820ce8f15a11a9ed79fd73010e2625d0e1af4675f17b16f5ab6aa740fe743</citedby><cites>FETCH-LOGICAL-c795t-ffd9820ce8f15a11a9ed79fd73010e2625d0e1af4675f17b16f5ab6aa740fe743</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1480599/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1480599/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16789836$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Rice, Charles</contributor><creatorcontrib>Walters, Kathie-Anne</creatorcontrib><creatorcontrib>Joyce, Michael A</creatorcontrib><creatorcontrib>Thompson, Jill C</creatorcontrib><creatorcontrib>Smith, Maria W</creatorcontrib><creatorcontrib>Yeh, Matthew M</creatorcontrib><creatorcontrib>Proll, Sean</creatorcontrib><creatorcontrib>Zhu, Lin-Fu</creatorcontrib><creatorcontrib>Gao, T J</creatorcontrib><creatorcontrib>Kneteman, Norman M</creatorcontrib><creatorcontrib>Tyrrell, D Lorne</creatorcontrib><creatorcontrib>Katze, Michael G</creatorcontrib><title>Host-specific response to HCV infection in the chimeric SCID-beige/Alb-uPA mouse model: role of the innate antiviral immune response</title><title>PLoS pathogens</title><addtitle>PLoS Pathog</addtitle><description>The severe combined immunodeficiency disorder (SCID)-beige/albumin (Alb)-urokinase plasminogen activator (uPA) mouse containing a human-mouse chimeric liver is currently the only small animal model capable of supporting hepatitis C virus (HCV) infection. 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In summary, the nature of the initial interferon response to HCV infection may determine the extent of viral-mediated effects on host gene expression.</description><subject>Albumins</subject><subject>Animal models</subject><subject>Animals</subject><subject>Antibodies, Viral - biosynthesis</subject><subject>Bioinformatics - Computational Biology</subject><subject>Chimera</subject><subject>Gastroenterology - Hepatology</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Genetic aspects</subject><subject>Hepatitis</subject><subject>Hepatitis C</subject><subject>Hepatitis C - genetics</subject><subject>Hepatitis C - immunology</subject><subject>Hepatitis C - metabolism</subject><subject>Hepatocytes - transplantation</subject><subject>Host-virus relationships</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immunity, Innate</subject><subject>Infections</subject><subject>Lipid Metabolism</subject><subject>Liver - metabolism</subject><subject>Medical research</subject><subject>Mice</subject><subject>Mice, SCID - genetics</subject><subject>Mice, SCID - immunology</subject><subject>Mus (Mouse)</subject><subject>Oxidative Stress</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Signal Transduction - immunology</subject><subject>Urokinase-Type Plasminogen Activator - genetics</subject><subject>Virology</subject><subject>Viruses</subject><issn>1553-7374</issn><issn>1553-7366</issn><issn>1553-7374</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqVk12P1CAUhhujcdfVf2C0iYmJF52FUkrZC5PJ-DGTbNS46i2h9DDDpoUR6Ebv_eEyO3XdMXtjuIDA876Hc-Bk2VOMZpgwfHrpRm9lP9tuZZwhVCJE-b3sGFNKCkZYdf_W-ih7FMIlQhUmuH6YHeGaNbwh9XH2a-lCLMIWlNFG5R7C1tkAeXT5cvEtN1aDisbZtMrjBnK1MQP4RF4sVm-KFswaTud9W4yf5vngxqQcXAf9We5dD7nT1yJjrYyQSxvNlfGyz80wjBZuoj3OHmjZB3gyzSfZ13dvvyyWxfnH96vF_LxQjNNYaN3xpkQKGo2pxFhy6BjXHSMIIyjrknYIsNRVzajGrMW1prKtpWQV0sAqcpI93_tuexfEVMAgcNlwVDKGykSs9kTn5KXYejNI_1M4acT1hvNrIX00qgfRkZZJThhgjioiKe8wkrzhnKsWMdImr9dTtLEdoFNgY8r9wPTwxJqNWLsrgasmvSVPBi8nA---jxCiGExQ0PfSQiq1qBta0waRBL74B7w7t4lay3T99LIuRVU7SzHHFDdVxUiTqNkdVBodDEY5C9qk_QPBqwNBYiL8iGs5hiBWF5__g_1wyFZ7VnkXggd9UzmMxK4D_iQpdh0gpg5Isme3q_5XNH158htSDQHe</recordid><startdate>20060601</startdate><enddate>20060601</enddate><creator>Walters, Kathie-Anne</creator><creator>Joyce, Michael A</creator><creator>Thompson, Jill C</creator><creator>Smith, Maria W</creator><creator>Yeh, Matthew M</creator><creator>Proll, Sean</creator><creator>Zhu, Lin-Fu</creator><creator>Gao, T J</creator><creator>Kneteman, Norman M</creator><creator>Tyrrell, D Lorne</creator><creator>Katze, Michael G</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>ISN</scope><scope>ISR</scope><scope>3V.</scope><scope>7QL</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20060601</creationdate><title>Host-specific response to HCV infection in the chimeric SCID-beige/Alb-uPA mouse model: role of the innate antiviral immune response</title><author>Walters, Kathie-Anne ; Joyce, Michael A ; Thompson, Jill C ; Smith, Maria W ; Yeh, Matthew M ; Proll, Sean ; Zhu, Lin-Fu ; Gao, T J ; Kneteman, Norman M ; Tyrrell, D Lorne ; Katze, Michael G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c795t-ffd9820ce8f15a11a9ed79fd73010e2625d0e1af4675f17b16f5ab6aa740fe743</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Albumins</topic><topic>Animal models</topic><topic>Animals</topic><topic>Antibodies, Viral - biosynthesis</topic><topic>Bioinformatics - Computational Biology</topic><topic>Chimera</topic><topic>Gastroenterology - Hepatology</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Genetic aspects</topic><topic>Hepatitis</topic><topic>Hepatitis C</topic><topic>Hepatitis C - genetics</topic><topic>Hepatitis C - immunology</topic><topic>Hepatitis C - metabolism</topic><topic>Hepatocytes - transplantation</topic><topic>Host-virus relationships</topic><topic>Humans</topic><topic>Immune response</topic><topic>Immunity, Innate</topic><topic>Infections</topic><topic>Lipid Metabolism</topic><topic>Liver - metabolism</topic><topic>Medical research</topic><topic>Mice</topic><topic>Mice, SCID - genetics</topic><topic>Mice, SCID - immunology</topic><topic>Mus (Mouse)</topic><topic>Oxidative Stress</topic><topic>Physiological aspects</topic><topic>Proteins</topic><topic>Rodents</topic><topic>Signal Transduction - immunology</topic><topic>Urokinase-Type Plasminogen Activator - genetics</topic><topic>Virology</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Walters, Kathie-Anne</creatorcontrib><creatorcontrib>Joyce, Michael A</creatorcontrib><creatorcontrib>Thompson, Jill C</creatorcontrib><creatorcontrib>Smith, Maria W</creatorcontrib><creatorcontrib>Yeh, Matthew M</creatorcontrib><creatorcontrib>Proll, Sean</creatorcontrib><creatorcontrib>Zhu, Lin-Fu</creatorcontrib><creatorcontrib>Gao, T J</creatorcontrib><creatorcontrib>Kneteman, Norman M</creatorcontrib><creatorcontrib>Tyrrell, D Lorne</creatorcontrib><creatorcontrib>Katze, Michael G</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Canada</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</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 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>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>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</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>Biological Science Database</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - 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This model was utilized to characterize the host transcriptional response to HCV infection. The purpose of these studies was to investigate the genetic component of the host response to HCV infection and also to distinguish virus-induced gene expression changes from adaptive HCV-specific immune-mediated effects. Gene expression profiles from HCV-infected mice were also compared to those from HCV-infected patients. Analyses of the gene expression data demonstrate that host factors regulate the response to HCV infection, including the nature of the innate antiviral immune response. They also indicate that HCV mediates gene expression changes, including regulation of lipid metabolism genes, which have the potential to be directly cytopathic, indicating that liver pathology may not be exclusively mediated by HCV-specific adaptive immune responses. This effect appears to be inversely related to the activation of the innate antiviral immune response. In summary, the nature of the initial interferon response to HCV infection may determine the extent of viral-mediated effects on host gene expression.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>16789836</pmid><doi>10.1371/journal.ppat.0020059</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Albumins Animal models Animals Antibodies, Viral - biosynthesis Bioinformatics - Computational Biology Chimera Gastroenterology - Hepatology Gene expression Gene Expression Profiling Genetic aspects Hepatitis Hepatitis C Hepatitis C - genetics Hepatitis C - immunology Hepatitis C - metabolism Hepatocytes - transplantation Host-virus relationships Humans Immune response Immunity, Innate Infections Lipid Metabolism Liver - metabolism Medical research Mice Mice, SCID - genetics Mice, SCID - immunology Mus (Mouse) Oxidative Stress Physiological aspects Proteins Rodents Signal Transduction - immunology Urokinase-Type Plasminogen Activator - genetics Virology Viruses |
| title | Host-specific response to HCV infection in the chimeric SCID-beige/Alb-uPA mouse model: role of the innate antiviral immune response |
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