{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T14:51:22Z","timestamp":1787064682166,"version":"build-2736575974"},"reference-count":61,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2013,11,8]],"date-time":"2013-11-08T00:00:00Z","timestamp":1383868800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Viral Hepatitis"],"published-print":{"date-parts":[[2013,12]]},"abstract":"<jats:title>Summary<\/jats:title>\n                  <jats:p>\n                    <jats:styled-content style=\"fixed-case\">APOBEC<\/jats:styled-content>\n                    3 (A3) cytidine deaminases are a family of enzymes that have been shown to inhibit the replication of\n                    <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>\n                    \u20101 and other retroviruses as part of the innate immune responses to virus infection. They can also hyperedit\n                    <jats:styled-content style=\"fixed-case\">HBV DNA<\/jats:styled-content>\n                    and inhibit\n                    <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>\n                    replication. Although A3 proteins are present at low levels in normal liver, A3 gene expression is highly stimulated by both interferon\u2010\u03b1 and interferon\u2010\u03b3. A3 deaminases are incorporated into nascent\n                    <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>\n                    capsids where they cleave amino groups from cytidine bases converting them to uracil in newly synthesized\n                    <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content>\n                    following reverse transcription of pregenomic\n                    <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                    . This modified\n                    <jats:styled-content style=\"fixed-case\">HBV DNA<\/jats:styled-content>\n                    is susceptible to degradation, or alternatively, numerous G\u2010to\u2010A nucleotide mutations are incorporated into positive\u2010strand viral\n                    <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content>\n                    disrupting coding sequences. A3 proteins in which the cytidine deaminase activity has been lost can also inhibit\n                    <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>\n                    replication, suggesting that there may be more than one way in which inhibition can occur. There is also evidence that A3 proteins might play a role in the development of hepatocellular carcinoma during chronic\n                    <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>\n                    infection.\n                  <\/jats:p>","DOI":"10.1111\/jvh.12192","type":"journal-article","created":{"date-parts":[[2013,11,8]],"date-time":"2013-11-08T03:30:20Z","timestamp":1383881420000},"page":"821-828","source":"Crossref","is-referenced-by-count":45,"title":["The inhibition of hepatitis B virus by\n                    <scp>APOBEC<\/scp>\n                    cytidine deaminases"],"prefix":"10.1111","volume":"20","author":[{"given":"E. M.","family":"Janahi","sequence":"first","affiliation":[{"name":"Department of Biology College of Science University of Bahrain Sakhir Bahrain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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