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Treatment with lamivudine commonly leads to a mutation within the tyrosine-methionine-aspartate-aspartate (YMDD) motif in the reverse transcriptase region of the HBV polymerase gene. The primary mutation in this motif consists of the replacement of methionine by valine or isoleucine at the 204 codon, designated as M204V/I. The nomenclature M204V/I is preferred to YMDD because it conveys more accurate information regarding where the specific mutation has occurred.
At present, the target of choice is the HBV polymerase protein – an enzyme that plays an essential role in viral replication . Within its four functional regions (Figure 2), drug resistance to lamivudine is associated with mutations in the very conserved catalytic polymerase /reverse transcriptase domain of the gene , located specifically at a locus of four amino acids consisting of tyrosine-methionine-aspartate-aspartate.
[Show abstract] [Hide abstract] ABSTRACT: Tyrosine-methionine-aspartate-aspartate (YMDD) mutations were the main limitation of lamivudine (LAM) for treating chronic hepatitis B (CHB). The aim of this study was to evaluate whether LAM combined with IFN-a offer advantage over lamivudine monotherapy for the occurrence of YMDD mutations in CHB using a meta-analysis. We searched electronic databases and calculated the odds ratios (OR) with their 95% confidence intervals (CI) and pooled the results.
S? d? kháng thu?c kháng virus d?i v?i LMV dã du?c v?ch ra d?i v?i tyrosine-methionine-aspartate-aspartate (YMDD) ? v? trí trên vùng xúc tác ho?c vùng C thu?c P ORF c?a HBV (Hình 1). Các d?t bi?n kháng thu?c tiên phát d?n d?n s? thay th? methionine b?ng valine, isoleucine, dôi khi là serine, và là rtM204I/V/S du?c xác d?nh. M?c dù rtM204I có th? du?c tìm th?y m?t cách riêng bi?t nhung M204V/S ch? du?c tìm th?y v?i các thay d?i khác, d?c bi?t là rtL180M (? vùng B) [20, 21].
Also, HBV viral load was detected by Real-Time PCR. HBV genotypes and polymerase gene mutations were determined by direct sequencing of the polymerase gene of HBV. Phylogenetic tree was constructed using neighbor-joining (NJ) method. ,Background: Hepatitis B virus (HBV) is replicated through reverse transcription of polymerase gene. Lamivudine can postpone the clinical progression in Hepatitis B infected patients, but the long-term monotherapy causes the emerge of YMDD (tyrosine-methionine-aspartate-aspartate.
It is approved for use in children aged 2--17 years who have compensated liver disease from chronic hepatitis B. In a placebo-controlled trial in children who have chronic hepatitis B without HIV infection, lamivudine was well tolerated, with virologic response (clearance of HBV DNA and HBeAg) in 23% of children receiving 52 weeks of lamivudine therapy, compared with 13% in placebo recipients (679). Response rates were higher (35%) for children with baseline serum transaminases more than two times normal (679). In a 2-year, open-label extension of this study, 213 children who remained HBeAg-positive after 1 year of therapy were continued on lamivudine treatment; virologic response was seen in 21% of the original lamivudine recipients, compared with 30% of prior placebo recipients, indicating that additional clinical response could occur over time with prolonged treatment (680). However, longer duration of lamivudine therapy also was associated with progressive development of lamivudine-resistant HBV, with base pair substitutions at the tyrosine-methionine-aspartate-aspartate.