Abstract: Although three major ADV-resistant mutations of HBV are known, rtA181T/V and rtN236T, HBV mutations associated with ADV resistance have not been fully identified.
[Detection of HBV resistant mutations related to lamivudine, adefovir and entecavir by reverse hybridization technique].
Abstract: RESULTS: The specific probes of 10 codon positions related to HBV wild-type and resistant reference strains, including I169T, V173L, L180M, A181T, T184G, S202I, M204V, Q215S, N236T, M250V, were distinguished effectively by reverse hybridization method.
Abstract: To detect non-synonymous amino acid substitutions associated with lamivudine, adefovir and entecavir, 26 specific oligonucleotide probes covering ten different codon positions, I169T, V173L/G, L180M, A181T/V, PMID: 20646332
2010
Virology journal
Discussion: The selection pressure caused by adefovir can lead to upraise of the mutations rtA181V and rtN236T or rtI233V.
[Resistance mutation patterns of hepatitis B virus in patients with suboptimal response to adefovir dipivoxil therapy after lamivudine resistance].
Abstract: CONCLUSIONS: In the patients with suboptimal viral response to ADV therapy after LAM resistance, the ADV resistance mutation patterns of A181T+N236T, A181V and A181T could easily be selected during ADV monotherapy; while in the patients with combination therapy, the LAM resistance mutation patterns of M204V+L180M, M204V+L180M+L229V, M204I+L80I, and M204V+L180M+V207I were predominant, the ETV resistance mutation T184I/S and S202G
Hepatitis B virus reverse transcriptase sequence variant database for sequence analysis and mutation discovery.
Abstract: Among the 10 well-characterized N(t)RTI-resistance mutations, L80I/V, V173L, L180M, A181T, T184S, S202G and M204I/V were significantly associated with treatment with lamivudine, an l-nucleoside analog, and A181S/T/V and N236T were significantly associated with treatment with adefovir, an acyclic nucleoside phosphonate.
Method: We analyzed the following mutations at 10 well-characterized DRM positions L80IV, I169T, V173L, L180M, A181TV, T184SAILFG, S202GI, M204VIS, N236T, and M
Hepatitis B virus (HBV) subgenotypes C2 and B2 differ in lamivudine- and adefovir-resistance-associated mutational patterns in HBV-infected Chinese patients.
PMID: 20881176
2010
Journal of clinical microbiology
Abstract: The incidence of adefovir-resistant mutations was similar between the two subsets, but HBV/C2 inclined to show rtA181V (3.6% for C2 versus 0.9% for B2; P<0.01), while HBV/B2 inclined to show rtN236T (4.5% for versus 2.5% for C2; P<0.01).
Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil.
Method: In brief, serum HBV DNA was amplified by PCR and pyrosequenced to detect the following mutations of HBV polymerase: I169T, V173L, L180M, A181V/T, T184G/S/A/C, A194T, S202G/I, M204V/I, N236T, and M250V.
Result: The serum samples of these two patients were examined for ten HBV mutations (I169T, V173L, L180M, A181V/T, T184G/S/A/C, A194T
Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient.
Abstract: alanine aminotransferase (ALT) 60 IU/L, and emergence of drug resistance to ADV (rtN236T).
Table: N236T
Discussion: Actually,there has also been no significant relationship between primer drug resistance mutations (the YVDD variant and the rtN236T variant), and HBV DNA loads and ALT levels.
Discussion: But, the rtN236T mutation responsible for primer ADV drug resistance (besides rtA181V/T) found by LIPAwas never detected in direct sequencing.
Discussion: In our study, applied LIPA assays showed wild types for the N236 and M204 amino acid positions, and this finding suggests that wild-type virus strain
Telbivudine, a nucleoside analog inhibitor of HBV polymerase, has a different in vitro cross-resistance profile than the nucleotide analog inhibitors adefovir and tenofovir.
Abstract: Conversely, against HBV cell lines expressing adefovir resistance mutations N236T and A181V, or the A194T mutant associated with resistance to tenofovir, telbivudine remained active as shown by respective fold-changes of 0.5 (N236T) and 1.0 (A181V and A194T).
HBV mutation literature information.
PMID: 
2010
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