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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
5 clinical significance (e.g. vaccine escape, precore and antiviral-resistant mutations) and carry out
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
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
16 equence suppresses the transcription of both precore and core RNAs, and the creation of the HNF1 bind
23 s study, sequences of the HBV polymerase and precore/core coding regions in 26 HBV-infected patients
25 is derived from a translation product of the precore/core gene by two proteolytic cleavage events: re
26 ted antigen (HBcrAg), a composite antigen of precore/core gene including classical hepatitis B core p
27 cidate the impact of hepatitis B virus (HBV) precore/core gene mutations on spontaneous hepatitis B e
28 und that the woodchuck hepatitis virus (WHV) precore/core gene products (i.e., WHV core-related antig
29 e information on levels of each component of precore/core gene products as well as their biochemical
30 s study, a comprehensive characterization of precore/core gene products revealed that HBcrAg componen
31 ted antigen (HBcrAg), a mixture of the viral precore/core gene products, has emerged as one potential
34 yzed by direct sequencing of the hepatitis B precore/core gene to identify the nucleotide and amino a
37 e was no correlation between the presence of precore/core promoter mutations and liver disease or HBV
39 to determine the effects of HBV genotype and precore/core promoter mutations on IFN-alpha response in
40 shown that reversion of HBV mutations in the precore/core promoter region conferring an HBeAg-negativ
41 tudy were to determine the prevalence of HBV precore/core promoter variants in the United States and
42 he presence of microsomal membranes were the precore/core protein and a truncated product representin
44 staining may be caused by expression of the precore/core protein, some of which may be translocated
45 , consequently, directs the translation of a precore/core protein, which is secreted as e antigen (HB
46 sis of the kinetics of each component of the precore/core-related antigen, along with serum viral DNA
48 ed as e antigen (HBeAg) following removal of precore-derived signal peptide and the carboxyl terminus
49 niversally showed mutations in their genomic preCore domains impeding hepatitis B e antigen (HBeAg) p
50 d the ability of the hepatitis B virus (HBV) precore, envelope, and X gene products to modulate HBV r
54 e experiments suggest that expression of the precore gene may be important in the regulation of HBV r
55 r, transient or stable overexpression of the precore gene resulted in striking inhibition of HBV repl
58 ations enabled core protein translation from precore messenger RNA, which could rescue the replicatio
61 ining two ducklings, ratios of wild-type and precore mutant virus fluctuated, with wild-type virus sl
63 ence of a rapidly replicating variant of the precore mutant, since genomes cloned from the infected d
65 f DHBV may be analogous to the selection for precore mutants of HBV during chronic hepatitis in human
66 either independently or in combination with precore mutation G1896A were associated with the transit
72 The function of the hepatitis B virus (HBV) precore or HBeAg is largely unknown because it is not re
73 that the intracellular HBeAg, also known as precore or p22, inhibits the antiviral signaling of IFN-
76 conversion rates, mutational patterns in the precore (PC) and core promoter (CP) regions, severity of
78 related occurrence of flares to presence of precore (PC) and/or basal core promoter (BCP) mutants an
80 n HepG2 cells initiated by transduction with precore (PC), rtM204I, and wild-type (wt) HBV recombinan
82 with siRNA against the polyadenylation (PA), precore (PreC), and surface (S) regions, respectively, c
85 ich sheds light on the enigmatic function of precore protein in shaping HBV chronicity and provides a
86 ar form of HBeAg, previously reported as the precore protein intermediate (p22) without the N-termina
91 slightly extended 5' end to cover the entire precore region and, consequently, directs the translatio
93 ces in the number of basal core promoter and precore region mutations between patients with HCC and c
94 he hepatitis B virus DNA sequence around the precore region was determined from sera of 45 black Sout
95 lymerase and primers targeting the conserved precore region, the HBV clones thus generated are replic
96 for possessing two nonsense mutations in the precore region, which together with the core gene encode
100 otein (HBc) and HBeAg and, additionally, the precore-related antigen PreC, retaining the N-terminal s
101 and e antigen (HBeAg) and, additionally, the precore-related antigen, PreC, retaining the N-terminal
103 t HNF4 could stimulate the expression of the precore RNA and the core RNA from the core promoter of b
106 factor(s) and that the transcription of only precore RNA and, consequently, the expression of e antig
112 n the core promoter, suppresses specifically precore RNA transcription, and enhances viral replicatio
114 epatitis B e antigen (HBeAg), encoded by the precore RNA, mediates part of the inhibition of viral re
118 ORF that was truncated and fused to inverted precore sequences was found using RNAs from Hep3B cells.
119 y primer extension analysis, novel core- and precore-specific transcripts were induced by Dex which i
120 e percent of the patients with e-CHB had the precore stop codon mutation, and an additional 41% had c
121 ine-resistant mutations had reversion of the precore stop codon mutation; in 2 patients this was acco
124 ID(50%), 9% chronic) and for high doses of a precore WHeAg-minus mutant WHV8 clone (17% chronic).