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Basic Characteristics of Mutations
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Mutation Site
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131_133ins |
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Mutation Site Sentence
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RESULTS: Twenty-one preS/S-gene mutants were cloned from four sequential serum samples, including 13 mutants that were not previously documented: (1) sI/T126V+sG145R; (2) preS1 nt 3014-3198 deletion; (3) preS1 nt 3046-3177 deletion; (4) preS1 nt 3046-3177 deletion+s115-116 ""INGTST"" insertion; (5) preS1 nt 3046-3177 deletion+s115-116 ""INGTST"" insertion+sG145R; (6) preS1 nt 3115-3123 deletion+sQ129N; (7) preS1 nt 3115-3123 deletion+s126-127 ""RPCMNCTI"" insertion; (8) s115-116 ""INGTST"" insertion; (9) s115-116 ""INGTST"" insertion+sG145R; (10) s126-127 ""RPCMNCTI"" insertion; (11) preS1 nt 2848-2862 deletion+preS2 initiation codon M-->I; (12) s122-123 ""KSTGLCK"" insertion+sQ129N; and (13) preS2 initiation codon M-->I+s131-133TSM-->NST. |
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Mutation Level
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Amino acid level |
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Mutation Type
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Insertion |
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Gene/Protein/Region
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S |
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Standardized Encoding Gene
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S
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I; (12) s122-123 ""KSTGLCK"" insertion+sQ129N; and (13) preS2 initiation codon M-->I+s131-133TSM-->NST.
-->
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Genotype/Subtype
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C |
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Viral Reference
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Y18856
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Functional Impact and Mechanisms
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Disease
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Occult HBV Infection
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Immune
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Y |
I; (12) s122-123 ""KSTGLCK"" insertion+sQ129N; and (13) preS2 initiation codon M-->I+s131-133TSM-->NST.
-->
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Target Gene
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-
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Clinical and Epidemiological Correlations
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Clinical Information
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Y |
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Treatment
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- |
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Location
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China |
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Literature Information
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PMID
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27182775
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Title
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Characterization of Novel Hepatitis B Virus PreS/S-Gene Mutations in a Patient with Occult Hepatitis B Virus Infection
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Author
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Chen J,Liu Y,Zhao J,Xu Z,Chen R,Si L,Lu S,Li X,Wang S,Zhang K,Li J,Han J,Xu D
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Journal
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PloS one
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Journal Info
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2016 May 16;11(5):e0155654
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Abstract
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OBJECTIVE: The impact of hepatitis B virus (HBV) preS/S-gene mutations on occult HBV infection (OBI) is not fully understood. This study characterized multiple novel HBV preS/S-gene mutants obtained from an OBI patient. METHODS: PreS/S-gene mutants were analyzed by clonal sequencing. Viral replication and expression were analyzed by transfecting HBV genomic recombinants into HepG2 cells. RESULTS: Twenty-one preS/S-gene mutants were cloned from four sequential serum samples, including 13 mutants that were not previously documented: (1) sI/T126V+sG145R; (2) preS1 nt 3014-3198 deletion; (3) preS1 nt 3046-3177 deletion; (4) preS1 nt 3046-3177 deletion+s115-116 ""INGTST"" insertion; (5) preS1 nt 3046-3177 deletion+s115-116 ""INGTST"" insertion+sG145R; (6) preS1 nt 3115-3123 deletion+sQ129N; (7) preS1 nt 3115-3123 deletion+s126-127 ""RPCMNCTI"" insertion; (8) s115-116 ""INGTST"" insertion; (9) s115-116 ""INGTST"" insertion+sG145R; (10) s126-127 ""RPCMNCTI"" insertion; (11) preS1 nt 2848-2862 deletion+preS2 initiation codon M-->I; (12) s122-123 ""KSTGLCK"" insertion+sQ129N; and (13) preS2 initiation codon M-->I+s131-133TSM-->NST. The proportion of preS1 nt 3046-3177 deletion and preS2 initiation codon M-->I+s131-133TSM-->NST mutants increased in the viral pool with prolonged disease. The 13 novel OBI-related mutants showed a 51.2-99.9% decrease in HBsAg levels compared with that of the wild type. Additional N-glycosylation-associated mutations, sQ129N and s131-133TSM-->NST, but not s126-127 ""RPCMNCTI,"" greatly attenuated anti-HBs binding to HBsAg. Compared with the wild type, replication and surface antigen promoter II activity of the preS1 nt 3046-3177 deletion mutant decreased by 43.3% and 97.0%, respectively. CONCLUSION: PreS/S-gene mutations may play coordinated roles in the presentation of OBI and might be associated with disease progression. This has implications for HBV diagnosis and vaccine improvement.
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Sequence Data
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KR014142
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