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1 of the pregenomic 3.5-kb RNA relative to the precore 3.5-kb RNA.
2 g)-negative than in HBeAg-positive patients (precore, 38% vs. 9%; core promoter, 51% vs. 36%; respect
3  basal core promoter T1762/A1764 mutants and precore A1896 mutants also were included, then 100% of p
4                              The hepatitis B precore Ag (HBeAg) is a secreted nonparticulate version
5  clinical significance (e.g. vaccine escape, precore and antiviral-resistant mutations) and carry out
6 ime in the United Kingdom, HBeAg status, and precore and basal core promoter mutations.
7 examine the tolerogenic potential of the HBV precore and core (HBcAg) proteins, HBc/HBeAg-transgenic
8 e of e-CHB in Hong Kong and the frequency of precore and core promoter mutations in these patients.
9 ypes of hepatitis B virus were reported, and precore and core promoter mutations were found in approx
10 ians should be aware of the existence of HBV precore and core promoter variants and the clinical cond
11                           In conclusion, HBV precore and core promoter variants are not rare in the U
12 era were tested for HBV genotypes as well as precore and core promoter variants by line-probe assays.
13 s in the United States and the prevalence of precore and core promoter variants in patients with ALF
14                                              Precore and core promoter variants were found in 27% and
15                                              Precore and core promoter variants were more common in h
16 equence suppresses the transcription of both precore and core RNAs, and the creation of the HNF1 bind
17                                              Precore and/or core promoter variants were associated wi
18                                          HBV precore and/or core promoter variants were common among
19                Seven of these 9 patients had precore and/or core promoter variants.
20         Sera were tested for HBV genotyping, precore, and core promoter variants by line-probe assays
21  point mutations immediately upstream of the precore AUG codon.
22             The cellular localization of the precore/core and core proteins was studied by immunofluo
23 s study, sequences of the HBV polymerase and precore/core coding regions in 26 HBV-infected patients
24                                              Precore/core constructs with the wild-type phenotype res
25 is derived from a translation product of the precore/core gene by two proteolytic cleavage events: re
26 cidate the impact of hepatitis B virus (HBV) precore/core gene mutations on spontaneous hepatitis B e
27                          We analyzed the HBV precore/core gene sequences by cloning method in 33 chro
28              The HBV basal core promoter and precore/core gene sequences were also evaluated in subje
29 yzed by direct sequencing of the hepatitis B precore/core gene to identify the nucleotide and amino a
30 HNF-4), HNF-3, and fetoprotein factor to the precore/core promoter enhancer II region.
31 e was no correlation between the presence of precore/core promoter mutations and liver disease or HBV
32         Hepatitis B virus (HBV) genotype and precore/core promoter mutations have been implicated in
33 to determine the effects of HBV genotype and precore/core promoter mutations on IFN-alpha response in
34 shown that reversion of HBV mutations in the precore/core promoter region conferring an HBeAg-negativ
35 tudy were to determine the prevalence of HBV precore/core promoter variants in the United States and
36 he presence of microsomal membranes were the precore/core protein and a truncated product representin
37                      The significance of the precore/core protein being present in the nucleus is not
38  staining may be caused by expression of the precore/core protein, some of which may be translocated
39 , consequently, directs the translation of a precore/core protein, which is secreted as e antigen (HB
40                                            A precore-deficient mutant of duck hepatitis B virus (DHBV
41 ed as e antigen (HBeAg) following removal of precore-derived signal peptide and the carboxyl terminus
42 d the ability of the hepatitis B virus (HBV) precore, envelope, and X gene products to modulate HBV r
43                              Variants in the precore (G(1896)A) and core promoter (A(1762)T, G(1764)A
44                             The reduction of precore gene expression was accompanied by an increase i
45                          The function of the precore gene in the biology of hepadnaviruses is unknown
46 e experiments suggest that expression of the precore gene may be important in the regulation of HBV r
47 r, transient or stable overexpression of the precore gene resulted in striking inhibition of HBV repl
48                We found that ablation of the precore gene resulted in the generation of a hepatitis B
49 on and is not invariably associated with the precore HBV mutant.
50 ations enabled core protein translation from precore messenger RNA, which could rescue the replicatio
51 (hepatitis B e antigen [HBeAg]-positive) and precore mutant (HBeAg-negative) sequences.
52             Core protein expression from the precore mutant constructs was very much reduced, indicat
53 ining two ducklings, ratios of wild-type and precore mutant virus fluctuated, with wild-type virus sl
54                   In another four ducks, the precore mutant virus slowly replaced the wild-type virus
55 ence of a rapidly replicating variant of the precore mutant, since genomes cloned from the infected d
56 cks, the wild-type virus slowly replaced the precore mutant.
57 f DHBV may be analogous to the selection for precore mutants of HBV during chronic hepatitis in human
58                                Reversions of precore mutations A1762T/G1764A and G1896A were observed
59 ation between HCC and basal core promoter or precore mutations in genotype F.
60 d the effect of therapy on the status of HBV precore mutations.
61 for natural HBV infection and especially for precore-negative chronic hepatitis.
62                           The selection of a precore-negative strain of DHBV may be analogous to the
63  The function of the hepatitis B virus (HBV) precore or HBeAg is largely unknown because it is not re
64                                              Precore (PC) (G1896A) and basal core promoter (BCP) (A17
65      We investigated whether the presence of precore (PC) and basal core promoter (BCP) mutants befor
66 conversion rates, mutational patterns in the precore (PC) and core promoter (CP) regions, severity of
67  related occurrence of flares to presence of precore (PC) and/or basal core promoter (BCP) mutants an
68                                     The 1896 precore (PC) mutation is the most frequent cause of hepa
69 n HepG2 cells initiated by transduction with precore (PC), rtM204I, and wild-type (wt) HBV recombinan
70                Amplified basic core promoter/precore, pre-S/S, and whole genome were sequenced, analy
71 with siRNA against the polyadenylation (PA), precore (PreC), and surface (S) regions, respectively, c
72 we were unable to detect the presence of the precore protein and e antigen from CID variants.
73          These observations suggest that the precore protein can exert a dominant negative effect on
74                     The other produces a p25 precore protein that is targeted by a signal peptide to
75                    The pre-C RNAs encode the precore protein which is proteolytically processed to yi
76                        Overexpression of the precore protein, however, eliminated nucleocapsid partic
77 slightly extended 5' end to cover the entire precore region and, consequently, directs the translatio
78 V associated with the G1896A mutation in the precore region has a high prevalence.
79 ces in the number of basal core promoter and precore region mutations between patients with HCC and c
80 he hepatitis B virus DNA sequence around the precore region was determined from sera of 45 black Sout
81 lymerase and primers targeting the conserved precore region, the HBV clones thus generated are replic
82 for possessing two nonsense mutations in the precore region, which together with the core gene encode
83 or by nonsense or frameshift mutation in the precore region.
84 for mutations in the basal core promoter and precore regions.
85 reaction (PCR) with primers in the HBV S and precore regions.
86 nscription of two related RNA products named precore RNA and core RNA.
87 t HNF4 could stimulate the expression of the precore RNA and the core RNA from the core promoter of b
88 (HBV) controls the transcription of both the precore RNA and the core RNA.
89 moter that controls the transcription of the precore RNA and the core RNA.
90 factor(s) and that the transcription of only precore RNA and, consequently, the expression of e antig
91                                          The precore RNA codes for the secreted e antigen, while the
92  affect the WT core promoter, suppressed the precore RNA expression of the double mutant.
93                                          The precore RNA has a slightly extended 5' end to cover the
94           Hence, the specific suppression of precore RNA transcription by this frequent double-nucleo
95 n the core promoter, suppresses specifically precore RNA transcription, and enhances viral replicatio
96 stigated how this double mutation suppresses precore RNA transcription.
97 epatitis B e antigen (HBeAg), encoded by the precore RNA, mediates part of the inhibition of viral re
98 ifically suppresses the transcription of the precore RNA.
99  of the pregenomic RNA compared with that of precore RNA.
100 or the transcription of the core RNA and the precore RNA.
101 ORF that was truncated and fused to inverted precore sequences was found using RNAs from Hep3B cells.
102 y primer extension analysis, novel core- and precore-specific transcripts were induced by Dex which i
103 e percent of the patients with e-CHB had the precore stop codon mutation, and an additional 41% had c
104 ine-resistant mutations had reversion of the precore stop codon mutation; in 2 patients this was acco
105 ariant was detected in 16 (55%) patients and precore stop codon variant in 18 (62%) patients.
106                                              Precore variant was detected in 27% of patients and core
107 ID(50%), 9% chronic) and for high doses of a precore WHeAg-minus mutant WHV8 clone (17% chronic).

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