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hepatitis C virus enigma
Hepatitis C virus (HCV) has a high propensity to establish chronic infection with end-stage liver disease. The high turnover of virus particles and high transcription error rates due to lack of proof-reading function of the viral polymerase imply that HCV exists as quasispecies, thus enabling the vi...
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| Published in: | APMIS : acta pathologica, microbiologica et immunologica Scandinavica microbiologica et immunologica Scandinavica, 2009-05, Vol.117 (5-6), p.427-439 |
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| Language: | English |
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| cites | cdi_FETCH-LOGICAL-c5764-1af8e59566f259d73065a30a51b5c19a66c21010859dca0286d64e3e5b320fac3 |
| container_end_page | 439 |
| container_issue | 5-6 |
| container_start_page | 427 |
| container_title | APMIS : acta pathologica, microbiologica et immunologica Scandinavica |
| container_volume | 117 |
| creator | MYRMEL, HELGE ULVESTAD, ELLING ÅSJØ, BIRGITTA |
| description | Hepatitis C virus (HCV) has a high propensity to establish chronic infection with end-stage liver disease. The high turnover of virus particles and high transcription error rates due to lack of proof-reading function of the viral polymerase imply that HCV exists as quasispecies, thus enabling the virus to evade the host immune response. Clearance of the virus is characterized by a multispecific, vigorous and persistent T-cell response, whereas T-cell responses are weak, narrow and transient in patients who develop chronic infection. At present, standard treatment is a combination of pegylated interferon-α and ribavirin, with a sustained viral response rate of 40-80%, depending on genotype. The mechanisms for the observed synergistic effects of the two drugs are still not known in detail, but in addition to direct antiviral mechanisms, the immunomodulatory effects of both drugs seem to be important, with a shift from Th2- to Th1-cytokine profiles in successfully treated patients. This article describes virus-host relations in the natural course of HCV infection and during treatment. |
| doi_str_mv | 10.1111/j.1600-0463.2009.02454.x |
| format | article |
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The high turnover of virus particles and high transcription error rates due to lack of proof-reading function of the viral polymerase imply that HCV exists as quasispecies, thus enabling the virus to evade the host immune response. Clearance of the virus is characterized by a multispecific, vigorous and persistent T-cell response, whereas T-cell responses are weak, narrow and transient in patients who develop chronic infection. At present, standard treatment is a combination of pegylated interferon-α and ribavirin, with a sustained viral response rate of 40-80%, depending on genotype. The mechanisms for the observed synergistic effects of the two drugs are still not known in detail, but in addition to direct antiviral mechanisms, the immunomodulatory effects of both drugs seem to be important, with a shift from Th2- to Th1-cytokine profiles in successfully treated patients. This article describes virus-host relations in the natural course of HCV infection and during treatment.</description><identifier>ISSN: 0903-4641</identifier><identifier>EISSN: 1600-0463</identifier><identifier>DOI: 10.1111/j.1600-0463.2009.02454.x</identifier><identifier>PMID: 19400866</identifier><language>eng</language><publisher>Oxford, UK: Oxford, UK : Blackwell Publishing Ltd</publisher><subject>Antigens, CD - physiology ; Antiviral Agents - pharmacology ; Antiviral Agents - therapeutic use ; Biological Evolution ; Disease Progression ; Drug Synergism ; Hepacivirus - drug effects ; Hepacivirus - immunology ; Hepacivirus - pathogenicity ; Hepacivirus - physiology ; Hepatitis ; Hepatitis C virus ; Hepatitis C, Chronic - complications ; Hepatitis C, Chronic - immunology ; Hepatitis C, Chronic - virology ; Host-Pathogen Interactions - drug effects ; Host-Pathogen Interactions - immunology ; Humans ; immunology ; Interferon-alpha - pharmacology ; Interferon-alpha - therapeutic use ; Liver Cirrhosis - etiology ; Liver Neoplasms - etiology ; Polyethylene Glycols - pharmacology ; Polyethylene Glycols - therapeutic use ; Receptors, Virus - physiology ; Recombinant Proteins ; Ribavirin - pharmacology ; Ribavirin - therapeutic use ; T-Lymphocyte Subsets - drug effects ; T-Lymphocyte Subsets - immunology ; Tetraspanin 28 ; variability ; Viral Hepatitis Vaccines ; Viremia - immunology ; Viremia - virology ; virus ; Virus Replication ; viruses</subject><ispartof>APMIS : acta pathologica, microbiologica et immunologica Scandinavica, 2009-05, Vol.117 (5-6), p.427-439</ispartof><rights>2009 The Authors. Journal Compilation © 2009 APMIS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5764-1af8e59566f259d73065a30a51b5c19a66c21010859dca0286d64e3e5b320fac3</citedby><cites>FETCH-LOGICAL-c5764-1af8e59566f259d73065a30a51b5c19a66c21010859dca0286d64e3e5b320fac3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19400866$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MYRMEL, HELGE</creatorcontrib><creatorcontrib>ULVESTAD, ELLING</creatorcontrib><creatorcontrib>ÅSJØ, BIRGITTA</creatorcontrib><title>hepatitis C virus enigma</title><title>APMIS : acta pathologica, microbiologica et immunologica Scandinavica</title><addtitle>APMIS</addtitle><description>Hepatitis C virus (HCV) has a high propensity to establish chronic infection with end-stage liver disease. The high turnover of virus particles and high transcription error rates due to lack of proof-reading function of the viral polymerase imply that HCV exists as quasispecies, thus enabling the virus to evade the host immune response. Clearance of the virus is characterized by a multispecific, vigorous and persistent T-cell response, whereas T-cell responses are weak, narrow and transient in patients who develop chronic infection. At present, standard treatment is a combination of pegylated interferon-α and ribavirin, with a sustained viral response rate of 40-80%, depending on genotype. The mechanisms for the observed synergistic effects of the two drugs are still not known in detail, but in addition to direct antiviral mechanisms, the immunomodulatory effects of both drugs seem to be important, with a shift from Th2- to Th1-cytokine profiles in successfully treated patients. This article describes virus-host relations in the natural course of HCV infection and during treatment.</description><subject>Antigens, CD - physiology</subject><subject>Antiviral Agents - pharmacology</subject><subject>Antiviral Agents - therapeutic use</subject><subject>Biological Evolution</subject><subject>Disease Progression</subject><subject>Drug Synergism</subject><subject>Hepacivirus - drug effects</subject><subject>Hepacivirus - immunology</subject><subject>Hepacivirus - pathogenicity</subject><subject>Hepacivirus - physiology</subject><subject>Hepatitis</subject><subject>Hepatitis C virus</subject><subject>Hepatitis C, Chronic - complications</subject><subject>Hepatitis C, Chronic - immunology</subject><subject>Hepatitis C, Chronic - virology</subject><subject>Host-Pathogen Interactions - drug effects</subject><subject>Host-Pathogen Interactions - immunology</subject><subject>Humans</subject><subject>immunology</subject><subject>Interferon-alpha - pharmacology</subject><subject>Interferon-alpha - therapeutic use</subject><subject>Liver Cirrhosis - etiology</subject><subject>Liver Neoplasms - etiology</subject><subject>Polyethylene Glycols - pharmacology</subject><subject>Polyethylene Glycols - therapeutic use</subject><subject>Receptors, Virus - physiology</subject><subject>Recombinant Proteins</subject><subject>Ribavirin - pharmacology</subject><subject>Ribavirin - therapeutic use</subject><subject>T-Lymphocyte Subsets - drug effects</subject><subject>T-Lymphocyte Subsets - immunology</subject><subject>Tetraspanin 28</subject><subject>variability</subject><subject>Viral Hepatitis Vaccines</subject><subject>Viremia - immunology</subject><subject>Viremia - virology</subject><subject>virus</subject><subject>Virus Replication</subject><subject>viruses</subject><issn>0903-4641</issn><issn>1600-0463</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><recordid>eNqNkMtPwzAMxiMEYuNx5wQ7cWtxksZtDxymARtivASIo5V16cjYi2aF8d-T0mlc8cWW_PtsfR9jLQ4h93U2DjkCBBChDAVAGoKIVBSutlhzs9hmTUhBBhFGvMH2nBsDcJFgvMsaPI0AEsQmO3ozC720S-tandanLUrXMjM7muoDtpPriTOH677PXq4unzu9oH_fve60-0GmYowCrvPEqFQh5kKlw1gCKi1BKz5QGU81YiY4cEj8MtPg_w8xMtKogRSQ60zus9P67qKYf5TGLWlqXWYmEz0z89KRAKWEt-fBpAazYu5cYXJaFHaqi2_iQFUqNKbKPFXmqUqFflOhlZcer3-Ug6kZ_gnXMXjgvAa-7MR8__swtR9uq8nrg1pv3dKsNnpdvBPGMlb0eteli-Smi3HvkR49f1LzuZ6THhXW0cuTAC6Bo-CYxPIHOzKFWg</recordid><startdate>200905</startdate><enddate>200905</enddate><creator>MYRMEL, HELGE</creator><creator>ULVESTAD, ELLING</creator><creator>ÅSJØ, BIRGITTA</creator><general>Oxford, UK : Blackwell Publishing Ltd</general><general>Blackwell Publishing Ltd</general><scope>FBQ</scope><scope>BSCLL</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>7T5</scope><scope>7T7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope></search><sort><creationdate>200905</creationdate><title>hepatitis C virus enigma</title><author>MYRMEL, HELGE ; ULVESTAD, ELLING ; ÅSJØ, BIRGITTA</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5764-1af8e59566f259d73065a30a51b5c19a66c21010859dca0286d64e3e5b320fac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Antigens, CD - physiology</topic><topic>Antiviral Agents - pharmacology</topic><topic>Antiviral Agents - therapeutic use</topic><topic>Biological Evolution</topic><topic>Disease Progression</topic><topic>Drug Synergism</topic><topic>Hepacivirus - drug effects</topic><topic>Hepacivirus - immunology</topic><topic>Hepacivirus - pathogenicity</topic><topic>Hepacivirus - physiology</topic><topic>Hepatitis</topic><topic>Hepatitis C virus</topic><topic>Hepatitis C, Chronic - complications</topic><topic>Hepatitis C, Chronic - immunology</topic><topic>Hepatitis C, Chronic - virology</topic><topic>Host-Pathogen Interactions - drug effects</topic><topic>Host-Pathogen Interactions - immunology</topic><topic>Humans</topic><topic>immunology</topic><topic>Interferon-alpha - pharmacology</topic><topic>Interferon-alpha - therapeutic use</topic><topic>Liver Cirrhosis - etiology</topic><topic>Liver Neoplasms - etiology</topic><topic>Polyethylene Glycols - pharmacology</topic><topic>Polyethylene Glycols - therapeutic use</topic><topic>Receptors, Virus - physiology</topic><topic>Recombinant Proteins</topic><topic>Ribavirin - pharmacology</topic><topic>Ribavirin - therapeutic use</topic><topic>T-Lymphocyte Subsets - drug effects</topic><topic>T-Lymphocyte Subsets - immunology</topic><topic>Tetraspanin 28</topic><topic>variability</topic><topic>Viral Hepatitis Vaccines</topic><topic>Viremia - immunology</topic><topic>Viremia - virology</topic><topic>virus</topic><topic>Virus Replication</topic><topic>viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MYRMEL, HELGE</creatorcontrib><creatorcontrib>ULVESTAD, ELLING</creatorcontrib><creatorcontrib>ÅSJØ, BIRGITTA</creatorcontrib><collection>AGRIS</collection><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>APMIS : acta pathologica, microbiologica et immunologica Scandinavica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MYRMEL, HELGE</au><au>ULVESTAD, ELLING</au><au>ÅSJØ, BIRGITTA</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>hepatitis C virus enigma</atitle><jtitle>APMIS : acta pathologica, microbiologica et immunologica Scandinavica</jtitle><addtitle>APMIS</addtitle><date>2009-05</date><risdate>2009</risdate><volume>117</volume><issue>5-6</issue><spage>427</spage><epage>439</epage><pages>427-439</pages><issn>0903-4641</issn><eissn>1600-0463</eissn><abstract>Hepatitis C virus (HCV) has a high propensity to establish chronic infection with end-stage liver disease. The high turnover of virus particles and high transcription error rates due to lack of proof-reading function of the viral polymerase imply that HCV exists as quasispecies, thus enabling the virus to evade the host immune response. Clearance of the virus is characterized by a multispecific, vigorous and persistent T-cell response, whereas T-cell responses are weak, narrow and transient in patients who develop chronic infection. At present, standard treatment is a combination of pegylated interferon-α and ribavirin, with a sustained viral response rate of 40-80%, depending on genotype. The mechanisms for the observed synergistic effects of the two drugs are still not known in detail, but in addition to direct antiviral mechanisms, the immunomodulatory effects of both drugs seem to be important, with a shift from Th2- to Th1-cytokine profiles in successfully treated patients. This article describes virus-host relations in the natural course of HCV infection and during treatment.</abstract><cop>Oxford, UK</cop><pub>Oxford, UK : Blackwell Publishing Ltd</pub><pmid>19400866</pmid><doi>10.1111/j.1600-0463.2009.02454.x</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0903-4641 |
| ispartof | APMIS : acta pathologica, microbiologica et immunologica Scandinavica, 2009-05, Vol.117 (5-6), p.427-439 |
| issn | 0903-4641 1600-0463 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_20552024 |
| source | Wiley-Blackwell Read & Publish Collection |
| subjects | Antigens, CD - physiology Antiviral Agents - pharmacology Antiviral Agents - therapeutic use Biological Evolution Disease Progression Drug Synergism Hepacivirus - drug effects Hepacivirus - immunology Hepacivirus - pathogenicity Hepacivirus - physiology Hepatitis Hepatitis C virus Hepatitis C, Chronic - complications Hepatitis C, Chronic - immunology Hepatitis C, Chronic - virology Host-Pathogen Interactions - drug effects Host-Pathogen Interactions - immunology Humans immunology Interferon-alpha - pharmacology Interferon-alpha - therapeutic use Liver Cirrhosis - etiology Liver Neoplasms - etiology Polyethylene Glycols - pharmacology Polyethylene Glycols - therapeutic use Receptors, Virus - physiology Recombinant Proteins Ribavirin - pharmacology Ribavirin - therapeutic use T-Lymphocyte Subsets - drug effects T-Lymphocyte Subsets - immunology Tetraspanin 28 variability Viral Hepatitis Vaccines Viremia - immunology Viremia - virology virus Virus Replication viruses |
| title | hepatitis C virus enigma |
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