Suppression of hepatitis B virus replication mediated by hepatitis A-induced cytokine production
: Background: Acute hepatitis A virus (HAV) infection can cause severe hepatitis especially in patients with underlying chronic liver disease. In patients with pre‐existing chronic hepatitis B (HBV) acute HAV infection can suppress HBV replication. The exact mechanism of HBV suppression during acute...
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| Veröffentlicht in: | Liver (Copenhagen) 2001-02, Vol.21 (1), p.45-49 |
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| creator | Van Nunen, Andeltje B. Pontesilli, Oscar Uytdehaag, Fons Osterhaus, Albert D. M. E. De Man, Robert A. |
| description | : Background: Acute hepatitis A virus (HAV) infection can cause severe hepatitis especially in patients with underlying chronic liver disease. In patients with pre‐existing chronic hepatitis B (HBV) acute HAV infection can suppress HBV replication. The exact mechanism of HBV suppression during acute HAV infection is still a subject of debate. One mechanism may be the production of HAV infection‐induced cytokines leading to suppression of HBV replication and viral clearance. Aim: To evaluate cytokine production and HBV‐specific lympho‐proliferative responses (LPR) during acute HAV infection in a patient with chronic HBV infection‐clearing markers of active HBV replication. Design: Early detection of a case of acute HAV infection in an HBeAg‐positive, HBV DNA‐positive chronic HBV patient treated with lamivudine. Results: At the time of HAV infection a sharp peak in the gamma‐interferon (IFN‐γ) level occurred just before the rise in serum transaminase activity. This was subsequently followed by a decrease in HBV DNA and HBeAg below the limit of detection of the assay. However the HBV‐specific T‐cell response was not modified. After resolution of the acute HAV infection and withdrawal of antiviral therapy HBV replication relapsed. Conclusion: The sharp rise in IFN‐γ production mediated by the acute HAV infection may be pivotal in the suppression of HBV replication in chronic hepatitis B. |
| doi_str_mv | 10.1034/j.1600-0676.2001.210107.x |
| format | Article |
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M. E. ; De Man, Robert A.</creator><creatorcontrib>Van Nunen, Andeltje B. ; Pontesilli, Oscar ; Uytdehaag, Fons ; Osterhaus, Albert D. M. E. ; De Man, Robert A.</creatorcontrib><description>: Background: Acute hepatitis A virus (HAV) infection can cause severe hepatitis especially in patients with underlying chronic liver disease. In patients with pre‐existing chronic hepatitis B (HBV) acute HAV infection can suppress HBV replication. The exact mechanism of HBV suppression during acute HAV infection is still a subject of debate. One mechanism may be the production of HAV infection‐induced cytokines leading to suppression of HBV replication and viral clearance. Aim: To evaluate cytokine production and HBV‐specific lympho‐proliferative responses (LPR) during acute HAV infection in a patient with chronic HBV infection‐clearing markers of active HBV replication. Design: Early detection of a case of acute HAV infection in an HBeAg‐positive, HBV DNA‐positive chronic HBV patient treated with lamivudine. Results: At the time of HAV infection a sharp peak in the gamma‐interferon (IFN‐γ) level occurred just before the rise in serum transaminase activity. This was subsequently followed by a decrease in HBV DNA and HBeAg below the limit of detection of the assay. However the HBV‐specific T‐cell response was not modified. After resolution of the acute HAV infection and withdrawal of antiviral therapy HBV replication relapsed. Conclusion: The sharp rise in IFN‐γ production mediated by the acute HAV infection may be pivotal in the suppression of HBV replication in chronic hepatitis B.</description><identifier>ISSN: 0106-9543</identifier><identifier>EISSN: 1600-0676</identifier><identifier>DOI: 10.1034/j.1600-0676.2001.210107.x</identifier><identifier>PMID: 11169072</identifier><identifier>CODEN: LIVEDR</identifier><language>eng</language><publisher>Copenhagen: Munksgaard International Publishers</publisher><subject>Acute Disease ; acute hepatitis A ; alpha interferon ; Antiviral Agents - therapeutic use ; Biological and medical sciences ; Cells, Cultured ; chronic hepatitis B ; DNA, Viral - analysis ; gamma-interferon ; Hepatitis A - blood ; Hepatitis A - immunology ; Hepatitis B Core Antigens - blood ; Hepatitis B virus - genetics ; Hepatitis B virus - growth & development ; Hepatitis B virus - immunology ; Hepatitis B virus - isolation & purification ; Hepatitis B, Chronic - drug therapy ; Hepatitis B, Chronic - immunology ; Hepatovirus - immunology ; Hepatovirus - isolation & purification ; Human viral diseases ; Humans ; IL-10 ; IL-12 ; Infectious diseases ; Interferon-gamma - biosynthesis ; Lamivudine - therapeutic use ; lympho-proliferative response ; Lymphocyte Activation - immunology ; Male ; Medical sciences ; Superinfection - immunology ; TNF-alpha ; Viral diseases ; Viral hepatitis ; Viral Interference - immunology ; Virus Replication</subject><ispartof>Liver (Copenhagen), 2001-02, Vol.21 (1), p.45-49</ispartof><rights>2001 INIST-CNRS</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4877-f1db459cf9142c14af9a40a3a9919ad83a1526f340ac2e8bc8cb619198b889aa3</citedby><cites>FETCH-LOGICAL-c4877-f1db459cf9142c14af9a40a3a9919ad83a1526f340ac2e8bc8cb619198b889aa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1034%2Fj.1600-0676.2001.210107.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1034%2Fj.1600-0676.2001.210107.x$$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=853590$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11169072$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Van Nunen, Andeltje B.</creatorcontrib><creatorcontrib>Pontesilli, Oscar</creatorcontrib><creatorcontrib>Uytdehaag, Fons</creatorcontrib><creatorcontrib>Osterhaus, Albert D. M. E.</creatorcontrib><creatorcontrib>De Man, Robert A.</creatorcontrib><title>Suppression of hepatitis B virus replication mediated by hepatitis A-induced cytokine production</title><title>Liver (Copenhagen)</title><addtitle>Liver</addtitle><description>: Background: Acute hepatitis A virus (HAV) infection can cause severe hepatitis especially in patients with underlying chronic liver disease. In patients with pre‐existing chronic hepatitis B (HBV) acute HAV infection can suppress HBV replication. The exact mechanism of HBV suppression during acute HAV infection is still a subject of debate. One mechanism may be the production of HAV infection‐induced cytokines leading to suppression of HBV replication and viral clearance. Aim: To evaluate cytokine production and HBV‐specific lympho‐proliferative responses (LPR) during acute HAV infection in a patient with chronic HBV infection‐clearing markers of active HBV replication. Design: Early detection of a case of acute HAV infection in an HBeAg‐positive, HBV DNA‐positive chronic HBV patient treated with lamivudine. Results: At the time of HAV infection a sharp peak in the gamma‐interferon (IFN‐γ) level occurred just before the rise in serum transaminase activity. This was subsequently followed by a decrease in HBV DNA and HBeAg below the limit of detection of the assay. However the HBV‐specific T‐cell response was not modified. After resolution of the acute HAV infection and withdrawal of antiviral therapy HBV replication relapsed. Conclusion: The sharp rise in IFN‐γ production mediated by the acute HAV infection may be pivotal in the suppression of HBV replication in chronic hepatitis B.</description><subject>Acute Disease</subject><subject>acute hepatitis A</subject><subject>alpha interferon</subject><subject>Antiviral Agents - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Cells, Cultured</subject><subject>chronic hepatitis B</subject><subject>DNA, Viral - analysis</subject><subject>gamma-interferon</subject><subject>Hepatitis A - blood</subject><subject>Hepatitis A - immunology</subject><subject>Hepatitis B Core Antigens - blood</subject><subject>Hepatitis B virus - genetics</subject><subject>Hepatitis B virus - growth & development</subject><subject>Hepatitis B virus - immunology</subject><subject>Hepatitis B virus - isolation & purification</subject><subject>Hepatitis B, Chronic - drug therapy</subject><subject>Hepatitis B, Chronic - immunology</subject><subject>Hepatovirus - immunology</subject><subject>Hepatovirus - isolation & purification</subject><subject>Human viral diseases</subject><subject>Humans</subject><subject>IL-10</subject><subject>IL-12</subject><subject>Infectious diseases</subject><subject>Interferon-gamma - biosynthesis</subject><subject>Lamivudine - therapeutic use</subject><subject>lympho-proliferative response</subject><subject>Lymphocyte Activation - immunology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Superinfection - immunology</subject><subject>TNF-alpha</subject><subject>Viral diseases</subject><subject>Viral hepatitis</subject><subject>Viral Interference - immunology</subject><subject>Virus Replication</subject><issn>0106-9543</issn><issn>1600-0676</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkM1u1DAURq0K1E4Lr1AFIXWX4Bs7_tnRljJUmpYF0C5dx3GEp5kktROYeXscZTSwZGXru-d-VzoIvQOcASb0wzoDhnGKGWdZjjFkOWDAPNseocVh8gotYshSWVBygk5DWEeSUV4coxMAYBLzfIGevo19720IrmuTrk5-2l4PbnAhuUp-OT-GxNu-cSaGEdjYyunBVkm5-4e8TF1bjSbGZjd0z661Se-7mEw7b9DrWjfBvt2_Z-jH55vv11_S1dfl7fXlKjVUcJ7WUJW0kKaWQHMDVNdSU6yJlhKkrgTRUOSsJjEzuRWlEaZkEGeiFEJqTc7QxdwbT7-MNgxq44KxTaNb241BcVwIJgVEUM6g8V0I3taq926j_U4BVpNetVaTRDVJVJNeNetV27h7vj8yltHF3829zwi83wM6GN3UXrfGhQMnClJIHKmPM_XbNXb3__fV6vZh_seKdK5wYbDbQ4X2z4pxwgv1eL9U-fLTw93yUShK_gDDpaZN</recordid><startdate>200102</startdate><enddate>200102</enddate><creator>Van Nunen, Andeltje B.</creator><creator>Pontesilli, Oscar</creator><creator>Uytdehaag, Fons</creator><creator>Osterhaus, Albert D. M. E.</creator><creator>De Man, Robert A.</creator><general>Munksgaard International Publishers</general><general>Munksgaard</general><scope>BSCLL</scope><scope>IQODW</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>7X8</scope></search><sort><creationdate>200102</creationdate><title>Suppression of hepatitis B virus replication mediated by hepatitis A-induced cytokine production</title><author>Van Nunen, Andeltje B. ; Pontesilli, Oscar ; Uytdehaag, Fons ; Osterhaus, Albert D. M. E. ; De Man, Robert A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4877-f1db459cf9142c14af9a40a3a9919ad83a1526f340ac2e8bc8cb619198b889aa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Acute Disease</topic><topic>acute hepatitis A</topic><topic>alpha interferon</topic><topic>Antiviral Agents - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Cells, Cultured</topic><topic>chronic hepatitis B</topic><topic>DNA, Viral - analysis</topic><topic>gamma-interferon</topic><topic>Hepatitis A - blood</topic><topic>Hepatitis A - immunology</topic><topic>Hepatitis B Core Antigens - blood</topic><topic>Hepatitis B virus - genetics</topic><topic>Hepatitis B virus - growth & development</topic><topic>Hepatitis B virus - immunology</topic><topic>Hepatitis B virus - isolation & purification</topic><topic>Hepatitis B, Chronic - drug therapy</topic><topic>Hepatitis B, Chronic - immunology</topic><topic>Hepatovirus - immunology</topic><topic>Hepatovirus - isolation & purification</topic><topic>Human viral diseases</topic><topic>Humans</topic><topic>IL-10</topic><topic>IL-12</topic><topic>Infectious diseases</topic><topic>Interferon-gamma - biosynthesis</topic><topic>Lamivudine - therapeutic use</topic><topic>lympho-proliferative response</topic><topic>Lymphocyte Activation - immunology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Superinfection - immunology</topic><topic>TNF-alpha</topic><topic>Viral diseases</topic><topic>Viral hepatitis</topic><topic>Viral Interference - immunology</topic><topic>Virus Replication</topic><toplevel>online_resources</toplevel><creatorcontrib>Van Nunen, Andeltje B.</creatorcontrib><creatorcontrib>Pontesilli, Oscar</creatorcontrib><creatorcontrib>Uytdehaag, Fons</creatorcontrib><creatorcontrib>Osterhaus, Albert D. M. E.</creatorcontrib><creatorcontrib>De Man, Robert 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>MEDLINE - Academic</collection><jtitle>Liver (Copenhagen)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Van Nunen, Andeltje B.</au><au>Pontesilli, Oscar</au><au>Uytdehaag, Fons</au><au>Osterhaus, Albert D. M. E.</au><au>De Man, Robert A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Suppression of hepatitis B virus replication mediated by hepatitis A-induced cytokine production</atitle><jtitle>Liver (Copenhagen)</jtitle><addtitle>Liver</addtitle><date>2001-02</date><risdate>2001</risdate><volume>21</volume><issue>1</issue><spage>45</spage><epage>49</epage><pages>45-49</pages><issn>0106-9543</issn><eissn>1600-0676</eissn><coden>LIVEDR</coden><abstract>: Background: Acute hepatitis A virus (HAV) infection can cause severe hepatitis especially in patients with underlying chronic liver disease. In patients with pre‐existing chronic hepatitis B (HBV) acute HAV infection can suppress HBV replication. The exact mechanism of HBV suppression during acute HAV infection is still a subject of debate. One mechanism may be the production of HAV infection‐induced cytokines leading to suppression of HBV replication and viral clearance. Aim: To evaluate cytokine production and HBV‐specific lympho‐proliferative responses (LPR) during acute HAV infection in a patient with chronic HBV infection‐clearing markers of active HBV replication. Design: Early detection of a case of acute HAV infection in an HBeAg‐positive, HBV DNA‐positive chronic HBV patient treated with lamivudine. Results: At the time of HAV infection a sharp peak in the gamma‐interferon (IFN‐γ) level occurred just before the rise in serum transaminase activity. This was subsequently followed by a decrease in HBV DNA and HBeAg below the limit of detection of the assay. However the HBV‐specific T‐cell response was not modified. After resolution of the acute HAV infection and withdrawal of antiviral therapy HBV replication relapsed. Conclusion: The sharp rise in IFN‐γ production mediated by the acute HAV infection may be pivotal in the suppression of HBV replication in chronic hepatitis B.</abstract><cop>Copenhagen</cop><pub>Munksgaard International Publishers</pub><pmid>11169072</pmid><doi>10.1034/j.1600-0676.2001.210107.x</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acute Disease acute hepatitis A alpha interferon Antiviral Agents - therapeutic use Biological and medical sciences Cells, Cultured chronic hepatitis B DNA, Viral - analysis gamma-interferon Hepatitis A - blood Hepatitis A - immunology Hepatitis B Core Antigens - blood Hepatitis B virus - genetics Hepatitis B virus - growth & development Hepatitis B virus - immunology Hepatitis B virus - isolation & purification Hepatitis B, Chronic - drug therapy Hepatitis B, Chronic - immunology Hepatovirus - immunology Hepatovirus - isolation & purification Human viral diseases Humans IL-10 IL-12 Infectious diseases Interferon-gamma - biosynthesis Lamivudine - therapeutic use lympho-proliferative response Lymphocyte Activation - immunology Male Medical sciences Superinfection - immunology TNF-alpha Viral diseases Viral hepatitis Viral Interference - immunology Virus Replication |
| title | Suppression of hepatitis B virus replication mediated by hepatitis A-induced cytokine production |
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