Clinical and virological characteristics associated with severe acute hepatitis B.
PMID: 24930916
2014
Clinical microbiology and infection
Abstract: The 19 patients with severe or fulminant AVH-B more frequently than the 119 with a normal course stated intravenous drug use (63.2% versus 36.1%, p 0.04) and were HBV-DNA negative (31.6% versus 11.8%, p 0.03) and anti-hepatitis C virus (HCV) positive (57.9% versus 19.3%, p 0.0008); the prevalences of different HBV genotypes and of the rtM204V/I mutant were similar in these three forms of AVH-B.
Abstract: The HBV mutants in the polymerase region were sought in 110 (87%) patients by direct sequencing, and the rtM204V/I mutations also by an allele-specific PCR.
Impact of the rtI187V polymerase substitution of hepatitis B virus on viral replication and antiviral drug susceptibility.
PMID: 25028473
2014
The Journal of general virology
Abstract: Replication-competent HBV constructs containing rtI187V and combined with LAM-resistant (rtM204I, rtL180M/rtM204V) mutations were generated, and compared with WT, LAM-resistant single (rtM204I) or double (rtL180M/rtM204V) and ADV-resistant (rtN236T) clones.
Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir.
PMID: 25061278
2014
Drug design, development and therapy
Conclusion: HBV DNA levels gradually increased, and LAM-resistant virus emerged (reverse transcriptase [rt] M204I).
Conclusion: In October 2007 (after switching from LAM to ETV), an amino acid substitution of the rt gene, rtM204I (LAM resistance substitution), was detected.
Hepatitis B virus sub-genotype A1 infection is characterized by high replication levels and rapid emergence of drug resistance in HIV-positive adults receiving first-line antiretroviral therapy in Malawi.
Abstract: At 6 months, M204I was detected in 8/46 (17%) and 16/17 (94%) subjects using Sanger and deep sequencing, respectively.
Performance of LigAmp assay for sensitive detection of drug-resistant hepatitis B virus minor variants in comparison with standard nucleotide sequencing.
Abstract: Among these subjects, rtM204V and rtM204I (ATT) mutations were identified by standard sequencing in 10 (25%) and 12 (30%) subjects, respectively.
Abstract: CONCLUSIONS: This data shows significantly higher sensitivity of LigAmp for detection of minority rtM204V and rtM204I (ATT) mutations over standard sequencing.
Abstract: LigAmp detected both rtM204V and rtM204I (ATT) mutations in 13 (32.5%) subjects, rtM204I mutation in 12 (30%) subjects and rt
Different mechanism of selection of adefovir-resistant mutant viruses during adefovir monotherapy in patients with lamivudine-resistant chronic hepatitis B.
Abstract: During ADV therapy, most rtM204V/I mutants were replaced by wild type in all 3 patients without the rtA181V/T mutation and in one patient with the rtA181V/T mutation.
Abstract: In patients with the rtA181V/T mutation (n = 6), the rtA181V/T mutant overtook the rtM204V/I mutant in 3 of 4 patients with ADV resistance.
Abstract: The majority of LMV-resistant mutants harbor the rtM204V/I mutation, while a minor fraction harbor the
A deep-sequencing method detects drug-resistant mutations in the hepatitis B virus in Indonesians.
Discussion: Moreover, the change of Leucine to Methionine has been described in association with other mutations in the YMDD polymerase domain, in particular with the substitutions rtM204V and rtM204I, related to interferon resistance and polymerase protein dysfunction.
Genetic insights on host and hepatitis B virus in liver diseases.
PMID: 25475418
2014
Mutation research. Reviews in mutation research
Abstract: We have described common mutations in the HBV genome (G1896A, rtM204V, rtM204I) which modulate the pathogenesis and carcinogenesis of the liver.
Establishment of drug-resistant HBV small-animal models by hydrodynamic injection.
Discussion: rtM204V/I are primary resistance mutations which mapped in conserved YMDD motif within C domain of the viral RT and facilitate ongoing viral DNA synthesis in the presence of LAM.
Discussion: When treating with LAM, drug resistance arises rapidly and amino acid substitutions compromise rtM204V/I, rtL180M and rtV173L, etc.
HBV mutation literature information.
PMID: 
2014
Clinical microbiology and infection
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