Is the course of perinatal hepatitis B virus infection influenced by genetic heterogeneity of the virus?
We studied the relations between genetic heterogeneity of pre‐C region of hepatitis B virus (HBV) DNA and outcome of HBV infection in 5 infants with perinatal infection, 3 born to antihepatitis B e antigen (HBeAg), and 2 to HBeAg positive mothers. HBV infection developed in the babies at 3–4 months...
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| Veröffentlicht in: | Journal of medical virology 1993-06, Vol.40 (2), p.87-90 |
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| container_title | Journal of medical virology |
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| creator | Raimondo, Giovanni Tanzi, Elisabetta Brancatelli, Santa Campo, Salvatore Sardo, Maria A. Rodinò, Giuseppina Pernice, Maurizio Zanetti, Alessandro R. |
| description | We studied the relations between genetic heterogeneity of pre‐C region of hepatitis B virus (HBV) DNA and outcome of HBV infection in 5 infants with perinatal infection, 3 born to antihepatitis B e antigen (HBeAg), and 2 to HBeAg positive mothers. HBV infection developed in the babies at 3–4 months of age, but it resolved with seroconversion to anti‐HBs in infants born to anti‐HBe positive mothers, while the infection became chronic in the 2 babies born to HBeAg positive mothers. HBV‐DNA extracted from the first hepatitis B surface antigen (HBsAg) positive serum sample of each baby was amplified and directly sequenced for the pre‐core region. HBV‐DNA sequences from 3 babies born to anti‐HBe positive mothers showed at position 1896 the contemporary presence of 2 nucleotides (G + A), indicating a mixture of wild‐type and "e minus"variant HBV. These findings suggest a possible co‐transmission of the 2 viruses from anti‐HBe positive mothers to newborns. HBV‐DNA from babies born to HBeAg positive mothers showed wild‐type sequences only. The results of this study suggest that the outcome of HBV infection in newborns depends not only on the host's immunocompetence and on viremia level in maternal blood, but also on heterogeneity of HBV. Transmission of mixed HBV populations appears associated with an early immunoelimination of the virus, while infection with wild‐type HBV alone contributes to induction of chronicity. © 1993 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/jmv.1890400202 |
| format | Article |
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HBV infection developed in the babies at 3–4 months of age, but it resolved with seroconversion to anti‐HBs in infants born to anti‐HBe positive mothers, while the infection became chronic in the 2 babies born to HBeAg positive mothers. HBV‐DNA extracted from the first hepatitis B surface antigen (HBsAg) positive serum sample of each baby was amplified and directly sequenced for the pre‐core region. HBV‐DNA sequences from 3 babies born to anti‐HBe positive mothers showed at position 1896 the contemporary presence of 2 nucleotides (G + A), indicating a mixture of wild‐type and "e minus"variant HBV. These findings suggest a possible co‐transmission of the 2 viruses from anti‐HBe positive mothers to newborns. HBV‐DNA from babies born to HBeAg positive mothers showed wild‐type sequences only. The results of this study suggest that the outcome of HBV infection in newborns depends not only on the host's immunocompetence and on viremia level in maternal blood, but also on heterogeneity of HBV. Transmission of mixed HBV populations appears associated with an early immunoelimination of the virus, while infection with wild‐type HBV alone contributes to induction of chronicity. © 1993 Wiley‐Liss, Inc.</description><identifier>ISSN: 0146-6615</identifier><identifier>EISSN: 1096-9071</identifier><identifier>DOI: 10.1002/jmv.1890400202</identifier><identifier>PMID: 8360636</identifier><identifier>CODEN: JMVIDB</identifier><language>eng</language><publisher>New York: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>"e minus" HBV ; Base Sequence ; Biological and medical sciences ; Carrier State - microbiology ; DNA, Viral - genetics ; Female ; HBV viability ; Hepatitis B - microbiology ; Hepatitis B - transmission ; Hepatitis B Antibodies - blood ; Hepatitis B e Antigens - blood ; Hepatitis B e Antigens - genetics ; Hepatitis B e Antigens - immunology ; hepatitis B virus ; Hepatitis B virus - genetics ; Human viral diseases ; Humans ; Infant, Newborn ; Infectious diseases ; Medical sciences ; Molecular Sequence Data ; Polymorphism, Genetic ; Pregnancy ; Pregnancy Complications, Infectious - microbiology ; Viral diseases ; Viral hepatitis ; wild-type HBV</subject><ispartof>Journal of medical virology, 1993-06, Vol.40 (2), p.87-90</ispartof><rights>Copyright © 1993 Wiley‐Liss, Inc., A Wiley Company</rights><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5332-f071d86c96b680c1b15269aff993c2a740ca629e2e94629715413b68099b56163</citedby><cites>FETCH-LOGICAL-c5332-f071d86c96b680c1b15269aff993c2a740ca629e2e94629715413b68099b56163</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%2Fjmv.1890400202$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjmv.1890400202$$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=4874314$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8360636$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Raimondo, Giovanni</creatorcontrib><creatorcontrib>Tanzi, Elisabetta</creatorcontrib><creatorcontrib>Brancatelli, Santa</creatorcontrib><creatorcontrib>Campo, Salvatore</creatorcontrib><creatorcontrib>Sardo, Maria A.</creatorcontrib><creatorcontrib>Rodinò, Giuseppina</creatorcontrib><creatorcontrib>Pernice, Maurizio</creatorcontrib><creatorcontrib>Zanetti, Alessandro R.</creatorcontrib><title>Is the course of perinatal hepatitis B virus infection influenced by genetic heterogeneity of the virus?</title><title>Journal of medical virology</title><addtitle>J. Med. Virol</addtitle><description>We studied the relations between genetic heterogeneity of pre‐C region of hepatitis B virus (HBV) DNA and outcome of HBV infection in 5 infants with perinatal infection, 3 born to antihepatitis B e antigen (HBeAg), and 2 to HBeAg positive mothers. HBV infection developed in the babies at 3–4 months of age, but it resolved with seroconversion to anti‐HBs in infants born to anti‐HBe positive mothers, while the infection became chronic in the 2 babies born to HBeAg positive mothers. HBV‐DNA extracted from the first hepatitis B surface antigen (HBsAg) positive serum sample of each baby was amplified and directly sequenced for the pre‐core region. HBV‐DNA sequences from 3 babies born to anti‐HBe positive mothers showed at position 1896 the contemporary presence of 2 nucleotides (G + A), indicating a mixture of wild‐type and "e minus"variant HBV. These findings suggest a possible co‐transmission of the 2 viruses from anti‐HBe positive mothers to newborns. HBV‐DNA from babies born to HBeAg positive mothers showed wild‐type sequences only. The results of this study suggest that the outcome of HBV infection in newborns depends not only on the host's immunocompetence and on viremia level in maternal blood, but also on heterogeneity of HBV. Transmission of mixed HBV populations appears associated with an early immunoelimination of the virus, while infection with wild‐type HBV alone contributes to induction of chronicity. © 1993 Wiley‐Liss, Inc.</description><subject>"e minus" HBV</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Carrier State - microbiology</subject><subject>DNA, Viral - genetics</subject><subject>Female</subject><subject>HBV viability</subject><subject>Hepatitis B - microbiology</subject><subject>Hepatitis B - transmission</subject><subject>Hepatitis B Antibodies - blood</subject><subject>Hepatitis B e Antigens - blood</subject><subject>Hepatitis B e Antigens - genetics</subject><subject>Hepatitis B e Antigens - immunology</subject><subject>hepatitis B virus</subject><subject>Hepatitis B virus - genetics</subject><subject>Human viral diseases</subject><subject>Humans</subject><subject>Infant, Newborn</subject><subject>Infectious diseases</subject><subject>Medical sciences</subject><subject>Molecular Sequence Data</subject><subject>Polymorphism, Genetic</subject><subject>Pregnancy</subject><subject>Pregnancy Complications, Infectious - microbiology</subject><subject>Viral diseases</subject><subject>Viral hepatitis</subject><subject>wild-type HBV</subject><issn>0146-6615</issn><issn>1096-9071</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1vEzEQxS0EKqFw5YbkA-K2wV87uz4hGkFbFOBAKdwsrzNLXDa7qe0t5L_HS6IgTj2NR_N7b0Z-hDznbM4ZE69vNndzXmumcsPEAzLjTEOhWcUfkhnjCgoAXj4mT2K8YYzVWogTclJLYCBhRtaXkaY1UjeMISIdWrrF4HubbEfXuLXJJx_pGb3zYYzU9y265Id-enUj9g5XtNnRH9hj8i4rEoZh6nzaTWaT9V_pm6fkUWu7iM8O9ZR8ff_uanFRLD-fXy7eLgtXSimKNh--qsFpaKBmjje8FKBt22otnbCVYs6C0ChQq1wrXiouJ1TrpgQO8pS82vtuw3A7Ykxm46PDrrM9DmM0VamFqpi8F-QAKsNlBud70IUhxoCt2Qa_sWFnODNTBiZnYP5lkAUvDs5js8HVET98ep6_PMxtdLZrg-2dj0dM1ZWSXGVM77FfvsPdPUvNh4_X_51Q7LU-Jvx91Nrw00Alq9J8-3RuFouL5fcvZ1fmWv4BNeWuNQ</recordid><startdate>199306</startdate><enddate>199306</enddate><creator>Raimondo, Giovanni</creator><creator>Tanzi, Elisabetta</creator><creator>Brancatelli, Santa</creator><creator>Campo, Salvatore</creator><creator>Sardo, Maria A.</creator><creator>Rodinò, Giuseppina</creator><creator>Pernice, Maurizio</creator><creator>Zanetti, Alessandro R.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</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>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>199306</creationdate><title>Is the course of perinatal hepatitis B virus infection influenced by genetic heterogeneity of the virus?</title><author>Raimondo, Giovanni ; Tanzi, Elisabetta ; Brancatelli, Santa ; Campo, Salvatore ; Sardo, Maria A. ; Rodinò, Giuseppina ; Pernice, Maurizio ; Zanetti, Alessandro R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5332-f071d86c96b680c1b15269aff993c2a740ca629e2e94629715413b68099b56163</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>"e minus" HBV</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Carrier State - microbiology</topic><topic>DNA, Viral - genetics</topic><topic>Female</topic><topic>HBV viability</topic><topic>Hepatitis B - microbiology</topic><topic>Hepatitis B - transmission</topic><topic>Hepatitis B Antibodies - blood</topic><topic>Hepatitis B e Antigens - blood</topic><topic>Hepatitis B e Antigens - genetics</topic><topic>Hepatitis B e Antigens - immunology</topic><topic>hepatitis B virus</topic><topic>Hepatitis B virus - genetics</topic><topic>Human viral diseases</topic><topic>Humans</topic><topic>Infant, Newborn</topic><topic>Infectious diseases</topic><topic>Medical sciences</topic><topic>Molecular Sequence Data</topic><topic>Polymorphism, Genetic</topic><topic>Pregnancy</topic><topic>Pregnancy Complications, Infectious - microbiology</topic><topic>Viral diseases</topic><topic>Viral hepatitis</topic><topic>wild-type HBV</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Raimondo, Giovanni</creatorcontrib><creatorcontrib>Tanzi, Elisabetta</creatorcontrib><creatorcontrib>Brancatelli, Santa</creatorcontrib><creatorcontrib>Campo, Salvatore</creatorcontrib><creatorcontrib>Sardo, Maria A.</creatorcontrib><creatorcontrib>Rodinò, Giuseppina</creatorcontrib><creatorcontrib>Pernice, Maurizio</creatorcontrib><creatorcontrib>Zanetti, Alessandro R.</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>Raimondo, Giovanni</au><au>Tanzi, Elisabetta</au><au>Brancatelli, Santa</au><au>Campo, Salvatore</au><au>Sardo, Maria A.</au><au>Rodinò, Giuseppina</au><au>Pernice, Maurizio</au><au>Zanetti, Alessandro R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Is the course of perinatal hepatitis B virus infection influenced by genetic heterogeneity of the virus?</atitle><jtitle>Journal of medical virology</jtitle><addtitle>J. Med. Virol</addtitle><date>1993-06</date><risdate>1993</risdate><volume>40</volume><issue>2</issue><spage>87</spage><epage>90</epage><pages>87-90</pages><issn>0146-6615</issn><eissn>1096-9071</eissn><coden>JMVIDB</coden><abstract>We studied the relations between genetic heterogeneity of pre‐C region of hepatitis B virus (HBV) DNA and outcome of HBV infection in 5 infants with perinatal infection, 3 born to antihepatitis B e antigen (HBeAg), and 2 to HBeAg positive mothers. HBV infection developed in the babies at 3–4 months of age, but it resolved with seroconversion to anti‐HBs in infants born to anti‐HBe positive mothers, while the infection became chronic in the 2 babies born to HBeAg positive mothers. HBV‐DNA extracted from the first hepatitis B surface antigen (HBsAg) positive serum sample of each baby was amplified and directly sequenced for the pre‐core region. HBV‐DNA sequences from 3 babies born to anti‐HBe positive mothers showed at position 1896 the contemporary presence of 2 nucleotides (G + A), indicating a mixture of wild‐type and "e minus"variant HBV. These findings suggest a possible co‐transmission of the 2 viruses from anti‐HBe positive mothers to newborns. HBV‐DNA from babies born to HBeAg positive mothers showed wild‐type sequences only. The results of this study suggest that the outcome of HBV infection in newborns depends not only on the host's immunocompetence and on viremia level in maternal blood, but also on heterogeneity of HBV. Transmission of mixed HBV populations appears associated with an early immunoelimination of the virus, while infection with wild‐type HBV alone contributes to induction of chronicity. © 1993 Wiley‐Liss, Inc.</abstract><cop>New York</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>8360636</pmid><doi>10.1002/jmv.1890400202</doi><tpages>4</tpages></addata></record> |
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| ispartof | Journal of medical virology, 1993-06, Vol.40 (2), p.87-90 |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | "e minus" HBV Base Sequence Biological and medical sciences Carrier State - microbiology DNA, Viral - genetics Female HBV viability Hepatitis B - microbiology Hepatitis B - transmission Hepatitis B Antibodies - blood Hepatitis B e Antigens - blood Hepatitis B e Antigens - genetics Hepatitis B e Antigens - immunology hepatitis B virus Hepatitis B virus - genetics Human viral diseases Humans Infant, Newborn Infectious diseases Medical sciences Molecular Sequence Data Polymorphism, Genetic Pregnancy Pregnancy Complications, Infectious - microbiology Viral diseases Viral hepatitis wild-type HBV |
| title | Is the course of perinatal hepatitis B virus infection influenced by genetic heterogeneity of the virus? |
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