Antiviral therapy for chronic hepatitis C: past, present, and future
Antiviral therapy for chronic hepatitis C has dramatically advanced since the discovery of the hepatitis C virus (HCV) in 1989 and the introduction of interferon (IFN) monotherapy in the early 1990s. The current standard therapy uses a combination of pegylated IFN and ribavirin. The duration of ther...
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Veröffentlicht in: | Journal of gastroenterology 2006-01, Vol.41 (1), p.17-27 |
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description | Antiviral therapy for chronic hepatitis C has dramatically advanced since the discovery of the hepatitis C virus (HCV) in 1989 and the introduction of interferon (IFN) monotherapy in the early 1990s. The current standard therapy uses a combination of pegylated IFN and ribavirin. The duration of therapy and response to therapy are HCV genotype-specific. Genotype 1 patients require 48 weeks of the combination therapy for 50% successful viral elimination, while genotype 2 patients require 24 weeks of therapy for 80% or 90% viral elimination. Early viral kinetics after the initiation of therapy is a useful predictor of the sustained virologic response (SVR), which is formally determined at 24 weeks after completion of the treatment. For example, an early virologic response, which is determined by a 2-log reduction of HCV RNA or viral elimination at 12 weeks after the initiation of therapy, is a strong negative predictor of SVR in genotype 1 patients. In contrast, a rapid virologic response of HCV RNA-negative at 4 weeks after the initiation of therapy identifies genotype 2 "super-responders," who may require a shorter period of therapy. Adherence to therapy is one of the most important factors for successful viral clearance. Hematopoietic growth factors such as epoetin and granulocyte-colony stimulating factor help reduce therapy-mediated cytopenia and improve patient compliance, thereby leading to better viral clearance. New types of anti-HCV agents such as HCV protease and polymerase inhibitors are needed for those patients that do not respond to combination therapy. |
doi_str_mv | 10.1007/s00535-005-1740-7 |
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The current standard therapy uses a combination of pegylated IFN and ribavirin. The duration of therapy and response to therapy are HCV genotype-specific. Genotype 1 patients require 48 weeks of the combination therapy for 50% successful viral elimination, while genotype 2 patients require 24 weeks of therapy for 80% or 90% viral elimination. Early viral kinetics after the initiation of therapy is a useful predictor of the sustained virologic response (SVR), which is formally determined at 24 weeks after completion of the treatment. For example, an early virologic response, which is determined by a 2-log reduction of HCV RNA or viral elimination at 12 weeks after the initiation of therapy, is a strong negative predictor of SVR in genotype 1 patients. In contrast, a rapid virologic response of HCV RNA-negative at 4 weeks after the initiation of therapy identifies genotype 2 "super-responders," who may require a shorter period of therapy. Adherence to therapy is one of the most important factors for successful viral clearance. Hematopoietic growth factors such as epoetin and granulocyte-colony stimulating factor help reduce therapy-mediated cytopenia and improve patient compliance, thereby leading to better viral clearance. New types of anti-HCV agents such as HCV protease and polymerase inhibitors are needed for those patients that do not respond to combination therapy.</description><identifier>ISSN: 0944-1174</identifier><identifier>EISSN: 1435-5922</identifier><identifier>DOI: 10.1007/s00535-005-1740-7</identifier><identifier>PMID: 16501853</identifier><language>eng</language><publisher>Japan: Springer Nature B.V</publisher><subject>Antiviral agents ; Antiviral Agents - therapeutic use ; Colony-stimulating factor ; Erythropoietin ; Genotype & phenotype ; Genotypes ; Growth factors ; Hepatitis C ; Hepatitis C, Chronic - drug therapy ; Humans ; Interferon ; Interferons - therapeutic use ; Leukocytes (granulocytic) ; Patients ; Proteinase inhibitors ; Ribavirin ; Treatment Outcome</subject><ispartof>Journal of gastroenterology, 2006-01, Vol.41 (1), p.17-27</ispartof><rights>Springer-Verlag Tokyo 2006</rights><rights>Springer-Verlag Tokyo 2006.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c473t-18fd54d89aad61c5fffbceaec14e73c5c543fe004bd0f0739f3c9e3ca04599e03</citedby><cites>FETCH-LOGICAL-c473t-18fd54d89aad61c5fffbceaec14e73c5c543fe004bd0f0739f3c9e3ca04599e03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786,27933,27934</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16501853$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hayashi, Norio</creatorcontrib><creatorcontrib>Takehara, Tetsuo</creatorcontrib><title>Antiviral therapy for chronic hepatitis C: past, present, and future</title><title>Journal of gastroenterology</title><addtitle>J Gastroenterol</addtitle><description>Antiviral therapy for chronic hepatitis C has dramatically advanced since the discovery of the hepatitis C virus (HCV) in 1989 and the introduction of interferon (IFN) monotherapy in the early 1990s. The current standard therapy uses a combination of pegylated IFN and ribavirin. The duration of therapy and response to therapy are HCV genotype-specific. Genotype 1 patients require 48 weeks of the combination therapy for 50% successful viral elimination, while genotype 2 patients require 24 weeks of therapy for 80% or 90% viral elimination. Early viral kinetics after the initiation of therapy is a useful predictor of the sustained virologic response (SVR), which is formally determined at 24 weeks after completion of the treatment. For example, an early virologic response, which is determined by a 2-log reduction of HCV RNA or viral elimination at 12 weeks after the initiation of therapy, is a strong negative predictor of SVR in genotype 1 patients. In contrast, a rapid virologic response of HCV RNA-negative at 4 weeks after the initiation of therapy identifies genotype 2 "super-responders," who may require a shorter period of therapy. Adherence to therapy is one of the most important factors for successful viral clearance. Hematopoietic growth factors such as epoetin and granulocyte-colony stimulating factor help reduce therapy-mediated cytopenia and improve patient compliance, thereby leading to better viral clearance. New types of anti-HCV agents such as HCV protease and polymerase inhibitors are needed for those patients that do not respond to combination therapy.</description><subject>Antiviral agents</subject><subject>Antiviral Agents - therapeutic use</subject><subject>Colony-stimulating factor</subject><subject>Erythropoietin</subject><subject>Genotype & phenotype</subject><subject>Genotypes</subject><subject>Growth factors</subject><subject>Hepatitis C</subject><subject>Hepatitis C, Chronic - drug therapy</subject><subject>Humans</subject><subject>Interferon</subject><subject>Interferons - therapeutic use</subject><subject>Leukocytes (granulocytic)</subject><subject>Patients</subject><subject>Proteinase inhibitors</subject><subject>Ribavirin</subject><subject>Treatment Outcome</subject><issn>0944-1174</issn><issn>1435-5922</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><recordid>eNp1kU1LxDAQhoMouq7-AC9SFDxZnTRJ03hb1k9Y8KLnkE0nbJduW5NW2H9vyi4IgpeZYeaZl2FeQi4o3FEAeR8ABBNpjCmVHFJ5QCaUx45QWXZIJqA4T2kcnZDTENYAlIEojskJzQXQQrAJeZw1ffVdeVMn_Qq96baJa31iV75tKpussDN91VchmT8knQn9bdJ5DNjEwjRl4oZ-8HhGjpypA57v85R8Pj99zF_TxfvL23y2SC2XrE9p4UrBy0IZU-bUCufc0qJBSzlKZoUVnDkE4MsSHEimHLMKmTXAhVIIbEpudrqdb78GDL3eVMFiXZsG2yHoXOYKsmwEr_-A63bwTbxNZ7niUuRZXkTq6l-KSppHSEaI7iDr2xA8Ot35amP8VlPQowt654KOUY8u6HHnci88LDdY_m7s385-AI3dgRs</recordid><startdate>200601</startdate><enddate>200601</enddate><creator>Hayashi, Norio</creator><creator>Takehara, Tetsuo</creator><general>Springer Nature 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>3V.</scope><scope>7RV</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>8BM</scope></search><sort><creationdate>200601</creationdate><title>Antiviral therapy for chronic hepatitis C: past, present, and future</title><author>Hayashi, Norio ; Takehara, Tetsuo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c473t-18fd54d89aad61c5fffbceaec14e73c5c543fe004bd0f0739f3c9e3ca04599e03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Antiviral agents</topic><topic>Antiviral Agents - therapeutic use</topic><topic>Colony-stimulating factor</topic><topic>Erythropoietin</topic><topic>Genotype & phenotype</topic><topic>Genotypes</topic><topic>Growth factors</topic><topic>Hepatitis C</topic><topic>Hepatitis C, Chronic - drug therapy</topic><topic>Humans</topic><topic>Interferon</topic><topic>Interferons - therapeutic use</topic><topic>Leukocytes (granulocytic)</topic><topic>Patients</topic><topic>Proteinase inhibitors</topic><topic>Ribavirin</topic><topic>Treatment Outcome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hayashi, Norio</creatorcontrib><creatorcontrib>Takehara, Tetsuo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma 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>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>ComDisDome</collection><jtitle>Journal of gastroenterology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hayashi, Norio</au><au>Takehara, Tetsuo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antiviral therapy for chronic hepatitis C: past, present, and future</atitle><jtitle>Journal of gastroenterology</jtitle><addtitle>J Gastroenterol</addtitle><date>2006-01</date><risdate>2006</risdate><volume>41</volume><issue>1</issue><spage>17</spage><epage>27</epage><pages>17-27</pages><issn>0944-1174</issn><eissn>1435-5922</eissn><abstract>Antiviral therapy for chronic hepatitis C has dramatically advanced since the discovery of the hepatitis C virus (HCV) in 1989 and the introduction of interferon (IFN) monotherapy in the early 1990s. The current standard therapy uses a combination of pegylated IFN and ribavirin. The duration of therapy and response to therapy are HCV genotype-specific. Genotype 1 patients require 48 weeks of the combination therapy for 50% successful viral elimination, while genotype 2 patients require 24 weeks of therapy for 80% or 90% viral elimination. Early viral kinetics after the initiation of therapy is a useful predictor of the sustained virologic response (SVR), which is formally determined at 24 weeks after completion of the treatment. For example, an early virologic response, which is determined by a 2-log reduction of HCV RNA or viral elimination at 12 weeks after the initiation of therapy, is a strong negative predictor of SVR in genotype 1 patients. In contrast, a rapid virologic response of HCV RNA-negative at 4 weeks after the initiation of therapy identifies genotype 2 "super-responders," who may require a shorter period of therapy. Adherence to therapy is one of the most important factors for successful viral clearance. Hematopoietic growth factors such as epoetin and granulocyte-colony stimulating factor help reduce therapy-mediated cytopenia and improve patient compliance, thereby leading to better viral clearance. New types of anti-HCV agents such as HCV protease and polymerase inhibitors are needed for those patients that do not respond to combination therapy.</abstract><cop>Japan</cop><pub>Springer Nature B.V</pub><pmid>16501853</pmid><doi>10.1007/s00535-005-1740-7</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Antiviral agents Antiviral Agents - therapeutic use Colony-stimulating factor Erythropoietin Genotype & phenotype Genotypes Growth factors Hepatitis C Hepatitis C, Chronic - drug therapy Humans Interferon Interferons - therapeutic use Leukocytes (granulocytic) Patients Proteinase inhibitors Ribavirin Treatment Outcome |
title | Antiviral therapy for chronic hepatitis C: past, present, and future |
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