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 HBV mutation literature information.


  Occult HBV Infection May Be Transmitted through Close Contact and Manifest as an Overt Infection.
 PMID: 26457811       2015       PloS one
Result: Amino acid substitutions in mother include T16I, R41S, V44A,N53S, H55R, W58R, N76D, S81T, V103I, G107E, N121I, I122L, N123D, Q125K, H126Y, N134D, N139H, N139Q, Y158H, I163V, F178L, S185N, V207M


  Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma.
 PMID: 25333524       2014       PloS one
Result: The L213I mutation (TTA to ATG) in surface leads to F221Y and A222T dual mutations in reverse transcriptase (RT) domain of HBV polymerase resulting a change in polymerase activity or viral replication whereas the mutation S98T in pre S1 (L12V in Polymerase) lies in the non-essential spacer region of the polymerase.
Discussion: One point mutation L213I observed in the overlapping surface and polymerase gene (


  Characterization of hepatitis virus B isolated from a multi-drug refractory patient.
 PMID: 20970466       2011       Virus research
Abstract: Several novel mutations, such as rtT128N, rtA222T, rtS256G, rtL271M, rtS332R, and rtN/T337D, were present in a majority of clones.


  Dynamics of hepatitis B virus resistance to entecavir in a nucleoside/nucleotide-naive patient.
 PMID: 18948142       2009       Antiviral research
Abstract: The lamivudine- and entecavir-resistant mutations emerged closely in combination with the rtV207L, rtA222T, rtP237T or rtI163V substitutions.


  [Mutation patterns in the RT region of hepatitis B virus P gene in patients treated with nucleoside/nucleotide analogs].
 PMID: 19497198       2009       Zhonghua gan zang bing za zhi
Abstract: Novel mutations, including A222T, L229V and S256C, were also found.


  Lamivudine and Famciclovir resistant hepatitis B virus associated with fatal hepatic failure.
 PMID: 12727536       2003       Journal of clinical virology
Abstract: Subsequent to the instigation of antiviral therapy, the dominant drug resistant HBV which caused virological breakthrough and was associated with hepatic failure displayed a series of unique mutations particularly in the BCP (A1762T and G1764A) and in the polymerase (rtL180M, rtM204V, rtA222T and rtL336V), core (cP5T, cS26A,



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