Abstract: Additionally, five polymorphic mutations, with a suggested role in drug resistance, were detected [rtQ215S (12.8%), rtI233V (4.3%), rtV214A (3.6%), rtV191I (0.7%), rtV207L (0.7%)].
Abstract: Amino acid changes at other six RT positions, potentially associated with resistance, were also analyzed (rtV84M-rtV191I-rtV207L-rtV2
Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection.
Abstract: A similar analysis of ten additional less well-characterized resistance mutations demonstrated a significant association with N(t)RTI treatment for four of the mutations: L82M, S85A, A200V, and Q215S.
Result:
Result: Among these ten less well-characterized mutations, three were polymorphic (prevalence >0.5%) in the 2,804 pooled untreated individuals: Q215S (1.1%), I233V (0.7%), and NASH238T (2.8%).
Result: For these mutations, a significant association with L-nucleosides was present for L82M, A200V and Q215S and an association with ANPs was present for S85A (Fisher's Exact test; Benjamini-Hochberg adjusted p value <0.01).
[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: 20549958
2010
Mikrobiyoloji bulteni
Abstract: Various mutations were detected in 34.1% (15/44) of CHB patients and these were identified as M2041 (n = 6), Q215S (n = 2), L801 + M2041 (n = 1), L80V + M2041 (n = 1), Q215S + M2041 (n = 1) and M2041 + L180M (n = 1) mutations responsible for LAM resistance; V214A (n = 1) and A181T + N236T (n = 1) mutations responsible for adefovir (ADV) resistance, and V84M + V173L (n = 1) mutation responsible for ADV + LAM resistance.
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: Interestingly, the treatment-naive patients had preexisting drug resistance mutations related to lamivudine (rtL180M+rtM204I), adefovir (rtA181V, rtQ215S, rtI233V), entecavir (intermediate susceptibility with rtL180M+rtM204IHBV variant), telbivudine (rtL180M+rtM204I), and tenofovir (rtA194T).
Naturally occurring amino-acid substitutions to nucleos(t)ide analogues in treatment naive Turkish patients with chronic hepatitis B.
Abstract: Each amino-acid substitution appeared alone and included rtA194T, rtV214A, rtQ215S, rtI233V and rtN236T.
Monitoring of therapy in patients with chronic hepatitis B virus.
PMID: 19550344
2010
European journal of gastroenterology & hepatology
Abstract: With regard to this case, the same results were observed by INNO-LiPA HBV DR v3 and direct sequencing, but by direct sequencing we detected an extra mutation rtQ215S that was present in two patients: one patient who was on treatment with LAM had an rtQ215S mutation in addition to an rtM204I, and the second patient treated with ADV had rtA181V.
[Entecavir resistance in entecavir naive lamivudine treated chronic hepatitis B patients].
Abstract: In these patients also rtL180M and rtQ215S mutations were detected as compensatory mutations and YVDD and YIDD variants were observed at the 204.
Prevalence, viral replication efficiency and antiviral drug susceptibility of rtQ215 polymerase mutations within the hepatitis B virus genome.
Abstract: BACKGROUND/AIMS: The rtQ215S mutation in the hepatitis B virus (HBV) polymerase has been described as a secondary mutation associated with resistance to lamivudine (LAM) and adefovir (ADV).
Abstract: Furthermore, rtQ215S, rtQ215P and rtQ215H harbouring constructs remained susceptible towards treatment with LAM or ADV in vitro.
Abstract: In phenotypic assays, rtQ215S, rtQ215P and rtQ215H constructs showed equivalent levels of viral replication as wi
HBV mutation literature information.
PMID: 
2011
Antiviral research
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