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Basic Characteristics of Mutations
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Mutation Site
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Q130P |
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Mutation Site Sentence
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The reverse transcriptase domain of the HBV DNA polymerase contained polymorphic exchanges rtA21S and rtQ130P, but no resistance-associated mutations. |
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Mutation Level
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Amino acid level |
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Mutation Type
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Nonsynonymous substitution |
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Gene/Protein/Region
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RT |
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Standardized Encoding Gene
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P
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Genotype/Subtype
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D |
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Viral Reference
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X02496;M23138;AY721605
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Functional Impact and Mechanisms
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Disease
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Hepatitis B Virus Infection
Liver Diseases, Alcoholic
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Immune
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- |
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Target Gene
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-
|
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Clinical and Epidemiological Correlations
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Clinical Information
|
Y |
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Treatment
|
- |
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Location
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- |
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Literature Information
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PMID
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22313146
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Title
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Reactivation of hepatitis B virus with mutated hepatitis B surface antigen in a liver transplant recipient receiving a graft from an antibody to hepatitis B surface antigen- and antibody to hepatitis B core antigen-positive donor
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Author
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Blaich A,Manz M,Dumoulin A,Schuttler CG,Hirsch HH,Gerlich WH,Frei R
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Journal
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Transfusion
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Journal Info
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2012 Sep;52(9):1999-2006
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Abstract
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BACKGROUND: Fresh-frozen plasma (FFP) may contain antibodies to hepatitis B surface antigen (HBsAg, anti-HBs). These anti-HBs may lead to a misinterpretation of the actual hepatitis B immune status. Furthermore, they may not only confer protection against hepatitis B virus (HBV), but may also favor the selection of HBsAg mutants. CASE REPORT: We report a case of de novo HBV infection in a HBV-naive recipient with alcoholic liver disease, who received a liver from a donor with antibodies to hepatitis B core antigen (HBcAg, anti-HBc) and anti-HBs. RESULTS: A lookback investigation revealed the following: 1) Due to anti-HBs passively acquired through FFP, the recipient was considered immune to HBV and did not receive anti-HBV prophylaxis. 2) Within 1 year after transplantation he developed hepatitis B in absence of any elevated liver enzymes after the anti-HBs by FFP declined. 3) Despite an infection with HBV-containing wild-type HBcAg, the patient did not seroconvert to anti-HBc positivity. 4) The replicating HBV encoded two HBsAg mutations, first sQ129R and 4 months later sP127S. They map to the highly conserved ""alpha"" determinant of the HBsAg loop. CONCLUSION: 1) Passive transfer of anti-HBs from FFP led to an erroneous pretransplant diagnosis of HBV immunity when the patient was in fact HBV-naive. 2) HBsAg mutations might have been selected in escape from donor's actively produced anti-HBs and the recipient's anti-HBs by FFP might have favored this selection. 3) It is doubtful whether hepatitis B immunoglobulin could have prevented the reactivation. 4) Antiviral prophylaxis would have been crucial.
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Sequence Data
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-
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