Characteristics of occult hepatitis B virus infection in the Solomon Islands.
PMID: 21455562
2011
International journal of molecular medicine
Abstract: Most of the HBV-DNA-positive individuals were infected with wild-type HBV, and only 3 strains demonstrated specific amino acid substitutions (P121X, T123N, C138S, P142S and D144E) in the alpha determinant region.
Monitoring of hepatitis B virus surface antigen escape mutations and concomitantly nucleos(t)ide analog resistance mutations in Turkish patients with chronic hepatitis B.
PMID: 20382061
2010
International journal of infectious diseases
Abstract: In the NUC therapy group the prevalence was 8.5% (12/142), with the following patterns: sY100C+sI110V, sL109I, sP120T, sP127T, sG130R+sG145X, sS132A+sY134N, sY134N+sG145R, s
Perinatal transmission of hepatitis B virus: an Australian experience.
PMID: 19413519
2009
The Medical journal of Australia
Abstract: The fourth mother-infant pair had an S gene variant, HBV D144E, which has been previously reported in association with vaccine/HBIG escape.
Molecular characterization of hepatitis B virus (HBV) isolates, including identification of a novel recombinant, in patients with acute HBV infection attending an Irish hospital.
Abstract: Variations within the S gene were identified in 6 isolates, including Gly145Ala, associated with vaccine immune escape, Asp144Glu, Ser143Leu and Phe134Leu, each associated with failure to detect HBsAg.
Antiviral resistance mutations potentiate hepatitis B virus immune evasion through disruption of its surface antigen a determinant.
Abstract: RESULTS: The mutations rtF166L/sF158Y (lamivudine-associated, compensatory) and rtl169T/sF161L (entecavir-associated, primary) acting alone, and the mutations rtV173L/sE164D (lamivudine-associated, compensatory) and rtSilent/sD144E (antibody escape-associated) each when combined with rtM204V/sl195M (lamivudine-associated, primary) led to decreases in antibody reactivity to epitopes in the first or second loop, or in both loops.
Evolution of hepatitis B virus sequence from a liver transplant recipient with rapid breakthrough despite hepatitis B immune globulin prophylaxis and lamivudine therapy.
1Abstract: These mutations caused L426I/L526M/M550I triple mutation (equivalent to L428I/L528M/M552I in previous reports) in the polymerase, and D144E mutation in the ""a"" determinant of HBsAg."
Abstract: Our study suggests that mutations in the HBsAg (D144E) and the polymerase (L426I/L526M/M550I) of HBV genome may be responsible for viral breakthrough despite HBIG prophylaxis and lamivudine therapy.
Abstract: Transfection experiments revealed that the
Reduced antigenicity of the hepatitis B virus HBsAg protein arising as a consequence of sequence changes in the overlapping polymerase gene that are selected by lamivudine therapy.
Abstract: HBsAg proteins containing the vaccine escape mutations G145R and D144E/G145R demonstrated markedly reduced binding to anti-HBs antibody.
"Restoration of replication phenotype of lamivudine-resistant hepatitis B virus mutants by compensatory changes in the ""fingers"" subdomain of the viral polymerase selected as a consequence of mutations in the overlapping S gene."
Abstract: In contrast, the HBV a determinant HBIg/vaccine escape mutants sP120T, sT123N, sG145R, and sD144E/G145R (that produce rtT128N, Q130P, rtW153Q, and rtG153E respectively) yielded as much virus as wild-type HBV while the sM133L (rtY141S) mutant was replication i
HBV mutation literature information.
PMID: 
2011
International journal of molecular medicine
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