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T J Harrison

Publications and source records attributed to T J Harrison.

At least 127 records · Page 7Linked to original sources
PubMed2001

Measurement of the B(0) and B(+) meson lifetimes with fully reconstructed hadronic final states.

The B(0) and B(+) meson lifetimes have been measured in e(+)e(-) annihilation data collected in 1999 and 2000 with the BABAR detector at center-of-mass energies near the Upsilon(4S) resonance. Events are selected in which one B meson is fully reconstructed in a hadronic final state while the second B meson is reconstructed inclusively. A combined fit to the B(0) and the B(+) decay time difference distributions yields tau(B(0)) = 1.546+/-0.032(stat)+/-0.022(syst) ps, tau(B(+)) = 1.673+/-0.032(stat)+/-0.023(syst) ps, and tau(B(+))/tau(B(0)) = 1.082+/-0.026(stat)+/-0.012(syst).

Journal Article↗
PubMed2001

Measurement of J/psi production in continuum e(+)e(-) annihilations near square root of s = 10.6 GeV.

The production of J/psi mesons in continuum e(+)e(-) annihilations has been studied with the BABAR detector at energies near the Upsilon(4S) resonance. The mesons are distinguished from J/psi production in B decays through their center-of-mass momentum and energy. We measure the cross section e(+)e(-)-->J/psi X to be 2.52+/-0.21+/-0.21 pb. We set a 90% C.L. upper limit on the branching fraction for direct Upsilon(4S)-->J/psi X decays at 4.7 x 10(-4).

Journal Article↗
PubMed2001

Measurement of branching fractions and search for CP-violating charge asymmetries in charmless two-body B decays into pions and kaons.

We present measurements, based on a sample of approximately 23x10(6) BB pairs, of the branching fractions and a search for CP-violating charge asymmetries in charmless hadronic decays of B mesons into two-body final states of kaons and pions. We find the branching fractions B(B0-->pi(+)pi(-)) = (4.1+/-1.0+/-0.7)x10(-6), B(B0-->K+pi(-)) = (16.7+/-1.6+/-1.3)x10(-6), B(B+-->K+pi(0)) = (10.8(+2.1)(-1.9)+/-1.0)x10(-6), B(B+-->K0pi(+)) = (18.2(+3.3)(-3.0)+/-2.0)x10(-6), B(B0-->K0pi(0)) = (8.2(+3.1)(-2.7)+/-1.2)x10(-6). We also report 90% confidence level upper limits for B meson decays to the pi(+)pi(0), K+K-, and K0K+ final states. In addition, charge asymmetries have been found to be consistent with zero, where the statistical precision is in the range of +/-0.10 to +/-0.18, depending on the decay mode.

Journal Article↗
PubMed2001

Measurement of the decays B--> phiK and B--> phiK*.

We have observed the decays B--> phiK and phiK(*) in a sample of over 45 million B mesons collected with the BABAR detector at the PEP-II collider. The measured branching fractions are B(B+--> phiK+) = (7.7(+1.6)(-1.4)+/-0.8)x10(-6), B(B0--> phiK0) = (8.1(+3.1)(-2.5)+/-0.8)x10(-6), B(B+--> phiK(*+)) = (9.7(+4.2)(-3.4)+/-1.7)x10(-6), and B(B0--> phiK(*0)) = (8.7(+2.5)(-2.1)+/-1.1)x10(-6). We also report the upper limit B(B+--> phipi(+))<1.4x10(-6) ( 90% C.L.).

Journal Article↗
PubMed2001

Observation of CP violation in the B(0) meson system.

We present an updated measurement of time-dependent CP-violating asymmetries in neutral B decays with the BABAR detector at the PEP-II asymmetric B Factory at SLAC. This result uses an additional sample of Upsilon(4S) decays collected in 2001, bringing the data available to 32 x 10(6) BB macro pairs. We select events in which one neutral B meson is fully reconstructed in a final state containing charmonium and the flavor of the other neutral B meson is determined from its decay products. The amplitude of the CP-violating asymmetry, which in the standard model is proportional to sin2 beta, is derived from the decay time distributions in such events. The result sin2 beta = 0.59+/-0.14(stat)+/-0.05(syst) establishes CP violation in the B(0) meson system. We also determine absolute value of lambda = 0.93+/-0.09(stat)+/-0.03(syst), consistent with no direct CP violation.

Journal Article↗
PubMed2001

Measurement of CP-violating asymmetries in B0 decays to CP eigenstates.

We present measurements of time-dependent CP-violating asymmetries in neutral B decays to several CP eigenstates. The measurement uses a data sample of 23x10(6) Upsilon(4S)-->BbarB decays collected by the BABAR detector at the PEP-II asymmetric B Factory at SLAC. In this sample, we find events in which one neutral B meson is fully reconstructed in a CP eigenstate containing charmonium and the flavor of the other neutral B meson is determined from its decay products. The amplitude of the CP-violating asymmetry, which in the standard model is proportional to sin2beta, is derived from the decay time distributions in such events. The result is sin2beta = 0.34+/-0.20 (stat)+/-0.05 (syst).

Journal Article↗
PubMed2001

Partial sequence analysis of indigenous hepatitis E virus isolated in the United Kingdom.

The first nucleotide sequences of hepatitis E virus (HEV) acquired in the United Kingdom are described. The sequences are novel and are related most closely to HEV isolated from Greece (Greece 2 strain), consistent with their having been derived from an indigenous European virus. HEV was assumed until recently to be rare in the United Kingdom and other industrialised countries and, consequently, hepatitis E may be under-diagnosed in industrialised countries.

Genotype↗
PubMed2001

Detection of sporadic cases of hepatitis E virus (HEV) infection in China using immunoassays based on recombinant open reading frame 2 and 3 polypeptides from HEV genotype 4.

We reported previously on the complete sequence of hepatitis E virus (HEV) genotype 4, isolated from patients with sporadic cases of acute HEV infection in China. At least eight HEV genotypes have now been described worldwide, and further isolates await classification. Current immunoassays for the detection of anti-HEV antibodies are based on polypeptides from genotypes 1 and 2 only and may be inadequate for the reliable detection of other genotypes. Because genotypes 1 and 4 predominate in China, we wished to investigate the antigenic reactivities of HEV genotype 4 proteins. Four overlapping regions of open reading frame 2 (ORF2) (FB5, amino acids [aa] 1 to 130; E4, aa 67 to 308; F2-2, aa 288 to 461; E5, aa 414 to 672) and the entire ORF3 product were expressed in Escherichia coli as fusion proteins. Enzyme immunoassays based on each of the five purified polypeptides were evaluated with sera from patients with sporadic cases of acute HEV infection. Individual immunoassays derived from HEV genotype 4 detected more cases of acute hepatitis E than a commercial assay. Some serum samples, which were positive for anti-HEV immunoglobulin G only by assays based on HEV genotype 4, were positive for HEV RNA by reverse transcription-PCR. Polypeptide FB5, from the N terminus of ORF2, had the greatest immunoreactivity with sera from patients with acute hepatitis E. These data indicate that the N terminus of ORF2 may provide epitopes which are highly reactive with acute-phase sera and that assays based on genotypes 1 and 2 alone may be inadequate for the detection of HEV infection in China, where sporadic cases of HEV infection are caused predominantly by HEV genotypes 4 and 1.

Acute Disease↗
PubMed2000

Unusual hepatitis B surface antigen variation in a child immunised against hepatitis B.

Perinatal transmission of and infection with hepatitis B (HBV) in early childhood are observed in a small proportion of the offspring of hepatitis B surface antigen (HBsAg)-positive mothers who are vaccinated against HBV immediately after giving birth. The children may be infected by wild-type HBV or by variants with amino acid substitutions in the "a" determinant of HBsAg, particularly at position 145 and, rarely, at positions 120, 126, 129, 131, 141, and 144. Four hundred and forty-six newborn infants of HBsAg-positive mothers in the northeastern part of the Czech Republic received combined active and passive immunisation against HBV. Only one child became an HBsAg carrier. This followed a mild, acute HBV illness in the beginning of the second year of his life. HBV DNA encoding the "a" determinant and surrounding region of HBsAg was sequenced after amplification from the plasma of the child and his mother. The child was infected with variants of HBsAg with substitutions at residues 137 and 139. The virus of the mother had changes at residues 120 and 121. HBV from both child and mother had an unusual substitution at residue 118 and seemed to be of the ayw subdeterminant.

Amino Acid Sequence↗
PubMed2000

The complete sequence of hepatitis E virus genotype 4 reveals an alternative strategy for translation of open reading frames 2 and 3.

Isolates of hepatitis E virus (HEV) have recently been described from China that are distinct from Burmese, Mexican and US viruses and constitute a novel genotype (genotype 4). Here, the complete genomic sequence of a representative isolate of genotype 4 HEV, amplified directly from the stool of an acutely infected patient, is presented. Analysis of the entire sequence confirms our previous conclusion, based upon partial sequence data, that these Chinese isolates belong to a novel genotype. Typical of genetic variation in HEV, most nucleotide substitutions occur in the third base of the codon and do not affect the amino acid sequence. The genotype 4 virus is unusual in that a single nucleotide insertion in the ORF 3 region changes the initiation of ORF 3, and perhaps also ORF 2. The consequences of these changes are discussed.

Adult↗
PubMed2000

Cytotoxic T lymphocyte responses and CTL epitope escape mutation in HBsAg, anti-HBe positive individuals.

BACKGROUND/AIMS: Clearance of hepatitis B virus (HBV) is characterised by a strong cytotoxic T cell response. Persistence of HBV in chronic hepatitis B carriers may be related to failure of this response. The aim of this study was to determine whether HLA class I restricted cytotoxic T lymphocyte (CTL) responses persist in anti-hepatitis B e (HBe) positive / HBV DNA negative individuals, and to correlate the presence of viral CTL epitope mutation with clinical outcome. METHODS: An HLA/HBV dual transfectant model was used to demonstrate these CTL responses in individuals chronically infected with HBV. Subsequently, a known hepatitis B core (HBc) CTL epitope was sequenced in a family of five chronically infected individuals all sharing a HLA allele (HLA-A68.1). RESULTS: Low level HLA class I restricted cytotoxic T cell responses were detected in the peripheral blood of five of eight anti-HBe positive individuals. In the family of HLA-A68.1 positive chronically infected individuals, mutation of the HLA-A68.1 restricted hepatitis B core antigen (HBcAg) CTL epitope STLPETTVVRR was found in all four anti-HBe positive individuals but not in the sole hepatitis B e antigen (HBeAg) positive patient. CONCLUSION: These data are consistent with a continued immune selection pressure on HBV in anti-HBe positive chronically infected individuals with low replicating HBV infection and suggest that mutation of a CTL epitope may be a consequence of the immune response, as opposed to the cause of viral persistence.

Adult↗
PubMed2000

[Mutation of hepatitis B virus DNA pre-C region in patients with primary hepatocellular carcinoma in Guangxi].

OBJECTIVE: To study the association between mutation of hepatitis B virus (HBV) pre-C gene and HBV infection in patients with primary hepatocellular carcinoma (PHC) but negative hepatitis B e antigen (HBeAg) in Guangxi Province, China. METHODS: Nested polymerase chain reaction (nPCR) was used for amplification of HBV DNA Pre C region in sera collected from 16 patients with PHC in Guangxi, and then their HBV DNA nPCR products were sequenced by Sanger method. RESULTS: Sera in fourteen of 16 patients showed positive HBV DNA, with a positive proportion of 87.5% (14/16). One (C23) of them was positive for HBeAg; one (C24) was negative HBeAg, but with normal sequence in his Pre C region; two (C7, C14) were co-infected with HBV wild and mutant strains; and the remainder eight cases (C3, C4, C5, C8, C10, C11, C12, C13) were infected with mutant virus strains, but stop codon at codon 28 was only found in C4, C5 and C12. One case (C8) was co-infected with both HBV stop codon mutant and non-stop codon strains. CONCLUSION: It is uncommon for patients with PHC in Guangxi infected with HBV mutant strain with classical mutation at nt 1 896, which suggests that maybe there exist other types of mutation other than that in pre-C region causing HBV infection without HBeAg.

Base Sequence↗
PubMed1999

A divergent genotype of hepatitis E virus in Chinese patients with acute hepatitis.

Recent studies have reported and provided nucleotide sequence data from divergent isolates of hepatitis E virus (HEV), including isolates from North America and Africa. Sera were investigated from 29 Chinese patients with a diagnosis of acute hepatitis and who were negative for hepatitis viruses A-E by serology (HEV was excluded by testing for IgG antibody only). To determine whether some patients were infected with HEV but had yet to seroconvert to antibody positivity, RT-PCR was carried out with primers designed within conserved sequences of the HEV open reading frame (ORF) 1 and ORF2 regions. Fifteen patients were found to harbour sequences related to HEV. Analysis of the HEV products revealed that nucleotide sequences from nine of the sera closely matched Burmese-like HEV sequences (more than 92% nucleotide identity across ORF1 and 88% in ORF2). The remaining six HEV isolates were similar to each other but divergent from all other known HEV sequences (74 to 83% nucleotide identity in ORF1 or ORF2). Phylogenetic analysis suggests that the six divergent isolates represent a fourth genotype of HEV, distinct from the previously described Burmese, Mexican and United States variants (genotypes 1, 2 and 3). This novel variant, referred to here as the Chinese genotype (genotype 4), may be responsible for a significant proportion of cases of acute hepatitis in China, as seen by the fact that 40% of the HEV-infected patients in this study were genotype 4 positive.

Acute Disease↗
PubMed1999

Functional analysis of mutations conferring lamivudine resistance on hepatitis B virus.

Two patterns of mutation are commonly observed in the polymerase gene of lamivudine [(-)2'-deoxy-3'-thiacytidine]-resistant hepatitis B virus (HBV). The M539I substitution in the conserved YMDD motif occurs independently of other changes, whereas the M539V substitution is associated with an additional upstream change (L515M). These mutations were introduced into a common background and their effects on HBV DNA replication and lamivudine resistance studied. The L515M and M539V mutations provided only partial resistance while the M539I mutation conferred a high degree of lamivudine resistance. The combination of the L515M and M539V mutations gave an intermediate level of replication competence, compared with either mutation alone, and increased resistance to lamivudine. This probably accounts for these two mutations always being observed together. The M539I mutation reduced replication competence.

Amino Acid Sequence↗
PubMed1999

Hepatitis E virus -- an update.

Hepatitis E virus (HEV) is the principal cause of enterically-transmitted, non-A, non-B hepatitis and has been associated with excess mortality in pregnant women infected during epidemics. Molecular cloning of the viral genome led to the development of diagnostic tests, including enzyme immunoassays for antibody and RT-PCR for viral RNA. Candidate vaccines have not yet reached clinical trials. The virus resembles caliciviruses, with a positive sense RNA genome encoding three open reading frames. The geographical distribution of the virus, which may infect domestic animals as well as humans, may be wider than thought originally.

Animals↗
PubMed1998

HBV core promoter mutations prevail in patients with hepatocellular carcinoma from Guangxi, China.

The development of primary liver cancer frequently is associated with persistent HBV infection, and tumours may arise in individuals who are anti-HBe positive. However, it is unclear whether viruses with an HBeAg-negative phenotype are associated with tumour development or are selected, during seroconversion, after chromosomal integration of wild-type viral DNA. In order to investigate the temporal evolution of the HBV genome in such individuals, the polymerase chain reaction was used to amplify HBV DNA from tumour tissue and serum of 14 patients from Guangxi, China with hepatocellular carcinoma. Comparison of nucleotide and amino acid sequences of the precore and proximal core region of HBV from the two sites in each patient produced evidence of divergence following integration in the tumour, but in most cases, HBeAg-negativity could not be explained by precore mutations. Sequences from the core promoter region were therefore examined and mutations were found in the majority, which are believed to upregulate transcription of the core (and pregenomic) RNA but to downregulate precore mRNA. To determine whether this finding merely reflected sequence variation among geographical isolates of HBV, the same region of HBV DNA from asymptomatic controls was sequenced and these mutations were found to be rare. We hypothesise that HBV with the core promoter mutations replicates at higher levels than the wild type, with the consequence that more integrations occur into the hepatocyte chromosomes during the early stages of infection. These hepatocytes may expand clonally and be targets for further mutagenic events leading to tumour development.

Adult↗
PubMed1998

GB virus C infection in patients with primary antibody deficiency.

Sera from 77 patients with common variable immunodeficiency (CVID) were tested for GB virus C (GBV-C) RNA, because they are prone to unexplained chronic hepatitis, and from 28 patients with X-linked agammaglobulinemia (XLA) who have a similar primary antibody deficiency but are not prone to hepatitis. Eight CVID and 8 XLA patients were positive; 6 positive CVID and 3 XLA patients had abnormal liver enzymes, explained in 3 by either hepatitis B or C virus infection. Most patients tested had antibodies to the E2 antigen of GBV-C, apparently passively acquired from their immunoglobulin therapy. The high prevalence of GBV-C viremia in CVID and XLA patients is probably explained by their long-term exposure to blood products. Our data indicate that GBV-C does not cause chronic hepatitis in immunocompromised XLA patients and is not the cause of chronic non-B or -C hepatitis in the majority of CVID patients.

Adult↗