Hepatitis C genotypes in patients with dual hepatitis B and C virus infection
In patients with chronic hepatitis B and C virus (HBV, HCV) infection, an inverse relationship in the replicative activity of the two viruses has been reported. In the present study the genotype of HCV was evaluated in 34 consecutive cases found with hepatitis B surface antigen (HBsAg) and anti‐HCV...
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Veröffentlicht in: | Journal of medical virology 1996-02, Vol.48 (2), p.157-160 |
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description | In patients with chronic hepatitis B and C virus (HBV, HCV) infection, an inverse relationship in the replicative activity of the two viruses has been reported. In the present study the genotype of HCV was evaluated in 34 consecutive cases found with hepatitis B surface antigen (HBsAg) and anti‐HCV in the serum, in order to identify its possible influence in determining the pattern of HBV/HCV interaction. Nineteen patients were HCV‐RNA positive and could be genotyped: 8 were infected by HCV‐1 (3 by HCV‐1a and 5 by HCV‐1b), 10 by HCV‐2, and only 1 by HCV‐3. Among these, 3 were HBV‐DNA positive, compared to 10 of 15 HCV‐RNA‐negative patients (P = 0.003), and all 3 were coinfected with HCV‐2.
Mean alanine aminotransferase (ALT) levels were similar between patients infected with HCV‐1 and HCV‐2. Among 7 patients with cirrhosis 5 were infected by HCV‐2, while 6 of 12 of those without cirrhosis had HCV‐1 infection.
In conclusion, HBV replication was inhibited more efficiently by HCV‐1 than by HCV‐2. Cirrhosis was frequently found in patients with dual HBV and HCV‐2 infection. © 1996 Wiley‐Liss, Inc. |
doi_str_mv | 10.1002/(SICI)1096-9071(199602)48:2<157::AID-JMV7>3.0.CO;2-8 |
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Mean alanine aminotransferase (ALT) levels were similar between patients infected with HCV‐1 and HCV‐2. Among 7 patients with cirrhosis 5 were infected by HCV‐2, while 6 of 12 of those without cirrhosis had HCV‐1 infection.
In conclusion, HBV replication was inhibited more efficiently by HCV‐1 than by HCV‐2. Cirrhosis was frequently found in patients with dual HBV and HCV‐2 infection. © 1996 Wiley‐Liss, Inc.</description><identifier>ISSN: 0146-6615</identifier><identifier>EISSN: 1096-9071</identifier><identifier>DOI: 10.1002/(SICI)1096-9071(199602)48:2<157::AID-JMV7>3.0.CO;2-8</identifier><identifier>PMID: 8835349</identifier><identifier>CODEN: JMVIDB</identifier><language>eng</language><publisher>New York: John Wiley & Sons, Inc</publisher><subject>Adult ; Biological and medical sciences ; Chronic Disease ; chronic hepatitis ; Female ; Genotype ; Hepacivirus - classification ; Hepacivirus - genetics ; Hepacivirus - immunology ; Hepacivirus - isolation & purification ; Hepatitis B - complications ; Hepatitis B - immunology ; Hepatitis B - physiopathology ; Hepatitis B - virology ; hepatitis B virus ; Hepatitis C - complications ; Hepatitis C - immunology ; Hepatitis C - physiopathology ; Hepatitis C - virology ; hepatitis C virus ; Human viral diseases ; Humans ; Infectious diseases ; Liver Diseases - physiopathology ; Liver Diseases - virology ; Male ; Medical sciences ; Middle Aged ; multiple virus infection ; Viral diseases ; Viral hepatitis ; viral interference</subject><ispartof>Journal of medical virology, 1996-02, Vol.48 (2), p.157-160</ispartof><rights>Copyright © 1996 Wiley‐Liss, Inc.</rights><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4587-46c4a110653d44a0aa2df0b7a47aea174d780071c9a34b030328143d560a47f03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2F%28SICI%291096-9071%28199602%2948%3A2%3C157%3A%3AAID-JMV7%3E3.0.CO%3B2-8$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2F%28SICI%291096-9071%28199602%2948%3A2%3C157%3A%3AAID-JMV7%3E3.0.CO%3B2-8$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2986454$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8835349$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pontisso, P.</creatorcontrib><creatorcontrib>Gerotto, M.</creatorcontrib><creatorcontrib>Ruvoletto, M. G.</creatorcontrib><creatorcontrib>Fattovich, G.</creatorcontrib><creatorcontrib>Chemello, L.</creatorcontrib><creatorcontrib>Tisminetzky, S.</creatorcontrib><creatorcontrib>Baralle, F.</creatorcontrib><creatorcontrib>Alberti, A.</creatorcontrib><title>Hepatitis C genotypes in patients with dual hepatitis B and C virus infection</title><title>Journal of medical virology</title><addtitle>J. Med. Virol</addtitle><description>In patients with chronic hepatitis B and C virus (HBV, HCV) infection, an inverse relationship in the replicative activity of the two viruses has been reported. In the present study the genotype of HCV was evaluated in 34 consecutive cases found with hepatitis B surface antigen (HBsAg) and anti‐HCV in the serum, in order to identify its possible influence in determining the pattern of HBV/HCV interaction. Nineteen patients were HCV‐RNA positive and could be genotyped: 8 were infected by HCV‐1 (3 by HCV‐1a and 5 by HCV‐1b), 10 by HCV‐2, and only 1 by HCV‐3. Among these, 3 were HBV‐DNA positive, compared to 10 of 15 HCV‐RNA‐negative patients (P = 0.003), and all 3 were coinfected with HCV‐2.
Mean alanine aminotransferase (ALT) levels were similar between patients infected with HCV‐1 and HCV‐2. Among 7 patients with cirrhosis 5 were infected by HCV‐2, while 6 of 12 of those without cirrhosis had HCV‐1 infection.
In conclusion, HBV replication was inhibited more efficiently by HCV‐1 than by HCV‐2. Cirrhosis was frequently found in patients with dual HBV and HCV‐2 infection. © 1996 Wiley‐Liss, Inc.</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Chronic Disease</subject><subject>chronic hepatitis</subject><subject>Female</subject><subject>Genotype</subject><subject>Hepacivirus - classification</subject><subject>Hepacivirus - genetics</subject><subject>Hepacivirus - immunology</subject><subject>Hepacivirus - isolation & purification</subject><subject>Hepatitis B - complications</subject><subject>Hepatitis B - immunology</subject><subject>Hepatitis B - physiopathology</subject><subject>Hepatitis B - virology</subject><subject>hepatitis B virus</subject><subject>Hepatitis C - complications</subject><subject>Hepatitis C - immunology</subject><subject>Hepatitis C - physiopathology</subject><subject>Hepatitis C - virology</subject><subject>hepatitis C virus</subject><subject>Human viral diseases</subject><subject>Humans</subject><subject>Infectious diseases</subject><subject>Liver Diseases - physiopathology</subject><subject>Liver Diseases - virology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>multiple virus infection</subject><subject>Viral diseases</subject><subject>Viral hepatitis</subject><subject>viral interference</subject><issn>0146-6615</issn><issn>1096-9071</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkV9v0zAUxS0EGqXwEZDygND2kHL9J7ZTJqSRsa7TSh8Y4_HKTRzmkSYlThj99ktoFR42aU-W7_3d4-N7CDmmMKEA7MPht3kyP6IQyzAGRQ9pHEtgR0JP2TGN1HR6Mj8NLxbX6hOfwCRZfmShfkZGw8BzMgIqZCgljV6SV97fAoCOGTsgB1rziIt4RBbndmMa1zgfJMFPW1bNdmN94MqgL9uy8cGda26CrDVFcDOwnwNTZt3EH1e3PZ3btHFV-Zq8yE3h7Zv9OSbfz75cJefh5XI2T04uw1REWoVCpsJQCjLimRAGjGFZDitlhDLWUCUypaH7QRobLlbAgTNNBc8iCR2SAx-T9zvdTV39bq1vcO18aovClLZqPSrNtVRUPglSBVTTDh-Tqx2Y1pX3tc1xU7u1qbdIAfs4EPs4sN8u9tvFXRwoNDLs4kDs4sA-DuQImCy7ci_7dv9-u1rbbBDd77_rv9v3jU9NkdemTJ0fMBZrKSLx392dK-z2gbUnnD1i7N-9kw13ss439u8ga-pfKBVXEf74OsMLmF2rxWmCC34PdVi-mg</recordid><startdate>199602</startdate><enddate>199602</enddate><creator>Pontisso, P.</creator><creator>Gerotto, M.</creator><creator>Ruvoletto, M. 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G.</creatorcontrib><creatorcontrib>Fattovich, G.</creatorcontrib><creatorcontrib>Chemello, L.</creatorcontrib><creatorcontrib>Tisminetzky, S.</creatorcontrib><creatorcontrib>Baralle, F.</creatorcontrib><creatorcontrib>Alberti, A.</creatorcontrib><collection>Istex</collection><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>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of medical virology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pontisso, P.</au><au>Gerotto, M.</au><au>Ruvoletto, M. G.</au><au>Fattovich, G.</au><au>Chemello, L.</au><au>Tisminetzky, S.</au><au>Baralle, F.</au><au>Alberti, A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hepatitis C genotypes in patients with dual hepatitis B and C virus infection</atitle><jtitle>Journal of medical virology</jtitle><addtitle>J. Med. Virol</addtitle><date>1996-02</date><risdate>1996</risdate><volume>48</volume><issue>2</issue><spage>157</spage><epage>160</epage><pages>157-160</pages><issn>0146-6615</issn><eissn>1096-9071</eissn><coden>JMVIDB</coden><abstract>In patients with chronic hepatitis B and C virus (HBV, HCV) infection, an inverse relationship in the replicative activity of the two viruses has been reported. In the present study the genotype of HCV was evaluated in 34 consecutive cases found with hepatitis B surface antigen (HBsAg) and anti‐HCV in the serum, in order to identify its possible influence in determining the pattern of HBV/HCV interaction. Nineteen patients were HCV‐RNA positive and could be genotyped: 8 were infected by HCV‐1 (3 by HCV‐1a and 5 by HCV‐1b), 10 by HCV‐2, and only 1 by HCV‐3. Among these, 3 were HBV‐DNA positive, compared to 10 of 15 HCV‐RNA‐negative patients (P = 0.003), and all 3 were coinfected with HCV‐2.
Mean alanine aminotransferase (ALT) levels were similar between patients infected with HCV‐1 and HCV‐2. Among 7 patients with cirrhosis 5 were infected by HCV‐2, while 6 of 12 of those without cirrhosis had HCV‐1 infection.
In conclusion, HBV replication was inhibited more efficiently by HCV‐1 than by HCV‐2. Cirrhosis was frequently found in patients with dual HBV and HCV‐2 infection. © 1996 Wiley‐Liss, Inc.</abstract><cop>New York</cop><pub>John Wiley & Sons, Inc</pub><pmid>8835349</pmid><doi>10.1002/(SICI)1096-9071(199602)48:2<157::AID-JMV7>3.0.CO;2-8</doi><tpages>4</tpages></addata></record> |
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subjects | Adult Biological and medical sciences Chronic Disease chronic hepatitis Female Genotype Hepacivirus - classification Hepacivirus - genetics Hepacivirus - immunology Hepacivirus - isolation & purification Hepatitis B - complications Hepatitis B - immunology Hepatitis B - physiopathology Hepatitis B - virology hepatitis B virus Hepatitis C - complications Hepatitis C - immunology Hepatitis C - physiopathology Hepatitis C - virology hepatitis C virus Human viral diseases Humans Infectious diseases Liver Diseases - physiopathology Liver Diseases - virology Male Medical sciences Middle Aged multiple virus infection Viral diseases Viral hepatitis viral interference |
title | Hepatitis C genotypes in patients with dual hepatitis B and C virus infection |
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