Prevalence and characterization of lamivudine-resistant hepatitis B virus mutations in HIV–HBV co-infected individuals

Cooley, Louise; Ayres, Anna; Bartholomeusz, Angeline; Lewin, Sharon R.; Crowe, Suzanne; Mijch, Anne M; Locarnini, Stephen; Sasadeusz, Joe

doi:10.1097/00002030-200307250-00009

Cited by 60 publications

(52 citation statements)

References 58 publications

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“…The triple mutation V519L/L526M/ M550V causes the concomitant amino acid substitutions E164D and I195M in the S protein. It has been shown recently that this triple mutant has a reduced affinity to anti-HBs antibodies, similarly to what happens with the well-known hepatitis B vaccine escape mutant G145R (Torresi et al 2002, Cooley et al 2003.…”

Section: Discussionmentioning

confidence: 70%

“…In contrast, all isolates from HBsAg negative samples did not display lamivudine resistance mutations. In another study involving HBsAg positive, HIV infected patients almost 50% of patients who were HBV DNA positive did not display lamivudine resistance mutations (Cooley et al 2003). Furthermore, these patients and those with resistance mutations had been under lamivudine therapy for a similar period of time.…”

Section: Discussionmentioning

confidence: 96%

“…In addition, one sample displayed a third, previously described (Torresi et al 2002, Cooley et al 2003 lamivudine resistance mutation, namely V519L. The triple mutation V519L/L526M/ M550V causes the concomitant amino acid substitutions E164D and I195M in the S protein.…”

Section: Discussionmentioning

confidence: 97%

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Patterns of hepatitis B virus infection in Brazilian human immunodeficiency virus infected patients: high prevalence of occult infection and low frequency of lamivudine resistant mutations

Sucupira

Mello

Santos

et al. 2006

Mem. Inst. Oswaldo Cruz

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Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 96%

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Patterns of hepatitis B virus infection in Brazilian human immunodeficiency virus infected patients: high prevalence of occult infection and low frequency of lamivudine resistant mutations

Sucupira

Mello

Santos

et al. 2006

Mem. Inst. Oswaldo Cruz

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“…HBV DNA was extracted and the catalytic domain of the reverse transcriptase/polymerase and the basal core promoter/precore regions were sequenced as previously described. 14,15 Liver Histology. Liver biopsy was also collected for formalin fixation and embedded in paraffin and processed for routine histology and hematoxylin-eosin staining.…”

Section: Methodsmentioning

confidence: 99%

The phenotype of hepatitis B virus-specific T cells differ in the liver and blood in chronic hepatitis B virus infection

et al. 2007

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H epatitis B virus (HBV)-specific T cells are im-portant in the successful clearance of acute HBV infection but also mediate liver damage in both acute and chronic HBV infections. In individuals with chronic HBV infection, circulating HBV-specific T cells are detected infrequently and are significantly reduced compared with individuals who recover from acute HBV infection. [1][2][3] We recently developed a sensitive method to assess HBV-specific T cells using an overlapping peptide library and intracellular cytokine staining (ICS). 4 However, despite detection of interferon-gamma (IFN-␥) HBV-specific T cells in blood, the magnitude of CD4 ϩ and CD8 ϩ HBV-specific T cells in chronic HBV infection was still significantly lower than that observed in other chronic infections such as human immunodeficiency virus (HIV)-1. 3,4 Previous studies using tetramer staining suggested a larger population of HBV-specific T cells being sequestered within the liver than in circulation. 2,5,6 Although a useful tool to quantify virus-specific T cells, the use of tetramers will detect virus-specific T cells regardless of their function or ability to produce cytokine. 7 In addition,

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“…The mutation at the rtM204V codon results in a change in the envelope gene at the sI195M codon, and the rtM204I mutation results in changes to the sW196L/S/Stop codon. In addition to these changes, the rtV173L mutation occurs in 9 to 22% of patients with LMV resistance (8,9). This mutation results in a change in the envelope gene at the sE164D codon.…”

Section: Hepatitis Delta Virus (Hdv) Is Encapsidated By the Envelope mentioning

confidence: 99%

Failure of the Lamivudine-Resistant rtM204I Hepatitis B Virus Mutants To Efficiently Support Hepatitis Delta Virus Secretion

Vietheer

Netter

Sozzi

et al. 2005

J Virol

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Hepatitis delta virus (HDV) is encapsidated by the envelope proteins of hepatitis B virus (HBV).The hepatitis delta virus (HDV) can cause severe chronic and acute hepatitis in humans (11). HDV coexists with hepatitis B virus (HBV) as it is dependent on the HBV envelope proteins for virus assembly. Inside the HBV envelope, the HDV virion contains a 1.7-kb circular RNA genome complexed with two HDV-encoded proteins, the large (214-aminoacid) and small (195-amino-acid) forms of hepatitis delta antigen (HDAg-L and HDAg-S, respectively) (22, 28). HDAg-L is crucial for virus assembly and interaction with the HBV envelope proteins (6). The other viral protein, HDAg-S, is essential for viral RNA replication (17).The HBV genome is approximately 3.2 kb and contains a number of overlapping reading frames. The HBV envelope consists of three surface proteins, small (hepatitis B surface antigen; HBsAg), middle, and large. All three HBV envelope proteins are encoded by a single open reading frame. The mRNA transcripts have different in-phase translational start codons and share a common stop codon, resulting in proteins with identical C-terminal ends and different N-terminal sequences. The HBsAg protein can form subviral particles that are secreted in excess in comparison to the HBV virion. The presence of HBsAg alone is sufficient for HDV assembly, although as with HBV, the large hepatitis B surface protein is required for infectivity. The envelope genes overlap the gene encoding the polymerase, and mutations may result in concomitant changes in both reading frames (21).The nucleoside analogue lamivudine (LMV) has been used for the treatment of hepatitis B infection (12,19,20). Lau and coworkers (18) demonstrated that although LMV is a potent inhibitor of HBV DNA replication, it did not inhibit HDV RNA replication or improve disease activity. Nevertheless, LMV is being used to treat hepatitis B infection in patients that are coinfected with HDV (4, 20, 29, 30). The major problem with LMV treatment has been the selection of HBV-resistant strains. In a study of long-term LMV treatment, HBV resistance was detected in 67% of patients after 4 years and 69% of patients after 5 years (19,20). Resistance to LMV is associated with a mutation in the reverse transcriptase (rt) region of the polymerase gene at the M204V/I codon (rtM204V/I), with or without an accompanying rtL180M mutation (according to the nomenclature by Stuyver and coworkers [24]) ( Table 1). The rtL180M change does not result in an amino acid change within the envelope protein. The concomitant HBsAg mutations selected by the antiviral agents are located towards the C-terminal region of the envelope protein. The mutation at the rtM204V codon results in a change in the envelope gene at the sI195M codon, and the rtM204I mutation results in changes to the sW196L/S/Stop codon. In addition to these changes, the rtV173L mutation occurs in 9 to 22% of patients with LMV resistance (8,9). This mutation results in a change in the envelope gene at the sE164D codon. Recently, Tor...

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Prevalence and characterization of lamivudine-resistant hepatitis B virus mutations in HIV–HBV co-infected individuals

Cited by 60 publications

References 58 publications

Patterns of hepatitis B virus infection in Brazilian human immunodeficiency virus infected patients: high prevalence of occult infection and low frequency of lamivudine resistant mutations

Patterns of hepatitis B virus infection in Brazilian human immunodeficiency virus infected patients: high prevalence of occult infection and low frequency of lamivudine resistant mutations

The phenotype of hepatitis B virus-specific T cells differ in the liver and blood in chronic hepatitis B virus infection

Failure of the Lamivudine-Resistant rtM204I Hepatitis B Virus Mutants To Efficiently Support Hepatitis Delta Virus Secretion

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