26 research outputs found
Illness perceptions and explanatory models of viral hepatitis B & C among immigrants and refugees: a narrative systematic review.
© 2015 Owiti et al.; licensee BioMed Central. This is an Open Access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain
Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article,
unless otherwise stated.BACKGROUND: Hepatitis B and C (HBV, HCV) infections are associated with high morbidity and mortality. Many countries with traditionally low prevalence (such as UK) are now planning interventions (screening, vaccination, and treatment) of high-risk immigrants from countries with high prevalence. This review aimed to synthesise the evidence on immigrants' knowledge of HBV and HCV that might influence the uptake of clinical interventions. The review was also used to inform the design and successful delivery of a randomised controlled trial of targeted screening and treatment. METHODS: Five databases (PubMed, CINHAL, SOCIOFILE, PsycINFO & Web of Science) were systematically searched, supplemented by reference tracking, searches of selected journals, and of relevant websites. We aimed to identify qualitative and quantitative studies that investigated knowledge of HBV and HCV among immigrants from high endemic areas to low endemic areas. Evidence, extracted according to a conceptual framework of Kleinman's explanatory model, was subjected to narrative synthesis. We adapted the PEN-3 model to categorise and analyse themes, and recommend strategies for interventions to influence help-seeking behaviour. RESULTS: We identified 51 publications including quantitative (n = 39), qualitative (n = 11), and mixed methods (n = 1) designs. Most of the quantitative studies included small samples and had heterogeneous methods and outcomes. The studies mainly concentrated on hepatitis B and ethnic groups of South East Asian immigrants residing in USA, Canada, and Australia. Many immigrants lacked adequate knowledge of aetiology, symptoms, transmission risk factors, prevention strategies, and treatment, of hepatitis HBV and HCV. Ethnicity, gender, better education, higher income, and English proficiency influenced variations in levels and forms of knowledge. CONCLUSION: Immigrants are vulnerable to HBV and HCV, and risk life-threatening complications from these infections because of poor knowledge and help-seeking behaviour. Primary studies in this area are extremely diverse and of variable quality precluding meta-analysis. Further research is needed outside North America and Australia
Determination of hydroxyl groups in biorefinery resources via quantitative 31P NMR spectroscopy
The analysis of chemical structural characteristics of biorefinery product streams (such as lignin and tannin) has advanced substantially over the past decade, with traditional wet-chemical techniques being replaced or supplemented by NMR methodologies. Quantitative 31P NMR spectroscopy is a promising technique for the analysis of hydroxyl groups because of its unique characterization capability and broad potential applicability across the biorefinery research community. This protocol describes procedures for (i) the preparation/solubilization of lignin and tannin, (ii) the phosphitylation of their hydroxyl groups, (iii) NMR acquisition details, and (iv) the ensuing data analyses and means to precisely calculate the content of the different types of hydroxyl groups. Compared with traditional wet-chemical techniques, the technique of quantitative 31P NMR spectroscopy offers unique advantages in measuring hydroxyl groups in a single spectrum with high signal resolution. The method provides complete quantitative information about the hydroxyl groups with small amounts of sample (~30 mg) within a relatively short experimental time (~30-120 min)
Interferon-Alpha Administration Enhances CD8+ T Cell Activation in HIV Infection
Type I interferons play important roles in innate immune defense. In HIV infection, type I interferons may delay disease progression by inhibiting viral replication while at the same time accelerating disease progression by contributing to chronic immune activation.To investigate the effects of type I interferons in HIV-infection, we obtained cryopreserved peripheral blood mononuclear cell samples from 10 subjects who participated in AIDS Clinical Trials Group Study 5192, a trial investigating the activity of systemic administration of IFNα for twelve weeks to patients with untreated HIV infection. Using flow cytometry, we examined changes in cell cycle status and expression of activation antigens by circulating T cells and their maturation subsets before, during and after IFNα treatment.The proportion of CD38+HLA-DR+CD8+ T cells increased from a mean of 11.7% at baseline to 24.1% after twelve weeks of interferon treatment (p = 0.006). These frequencies dropped to an average of 20.1% six weeks after the end of treatment. In contrast to CD8+ T cells, the frequencies of activated CD4+ T cells did not change with administration of type I interferon (mean percentage of CD38+DR+ cells = 2.62% at baseline and 2.17% after 12 weeks of interferon therapy). As plasma HIV levels fell with interferon therapy, this was correlated with a "paradoxical" increase in CD8+ T cell activation (p<0.001).Administration of type I interferon increased expression of the activation markers CD38 and HLA DR on CD8+ T cells but not on CD4+ T cells of HIV+ persons. These observations suggest that type I interferons may contribute to the high levels of CD8+ T cell activation that occur during HIV infection
Re-analysis of a human hepatitis B virus (HBV) isolate from an East African wild born Pan troglodytes schweinfurthii : Evidence for interspecies recombination between HBV infecting chimpanzee and human
According to current estimates, hepatitis B virus (HBV) has infected 2
billion people worldwide and among them, 360 million suffer from chronic
HBV infection. Except humans, HBV or HBV-like viruses have also been
isolated from different species of apes and mammals. Although
recombination has been described to occur extensively between different
genotypes within the human HBV lineage, no recombination event has ever
been reported between human and non-human primate HBV sequences. It was
our objective to perform an exhaustive search for recombination between
human and non-human primate HBV strains among all available full-length
human and non-human primate HBV sequences, using bootscanning and
phylogenetic analyses. Intriguingly, we found that an HBV sequence
isolated from a wild born Pan troglodytes schweinfurthii in East
Africa-FG-is a recombinant consisting of HBV infecting chimpanzee
(ChHBV) and human genotype C. More specifically, in a fragment of
approximately 500 nt (positions 551-1050 spanning half of the RT domain
of pol, which overlaps with half of the coding region of the small
surface protein), FG grouped with HBV genotype C, while in the rest of
the genome it grouped with ChHBV sequences. Phylogenetic analyses showed
that in the latter region FG was more closely related to the Pan
troglodytes troglodytes subspecies, forming an outlier to this group.
Moreover, we show evidence that the recombination event occurred after
the initial dispersion of HBV genotype C in humans. Finally, our
findings point out that although rare recombination between HBV viruses
infecting different species occurs. (c) 2004 Elsevier B.V. All rights
reserved
Re-analysis of a human hepatitis B virus (HBV) isolate from an East African wild born Pan troglodytes schweinfurthii: evidence for interspecies recombination between HBV infecting chimpanzee and human.
According to current estimates, hepatitis B virus (HBV) has infected 2 billion people worldwide and among them, 360 million suffer from chronic HBV infection. Except humans, HBV or HBV-like viruses have also been isolated from different species of apes and mammals. Although recombination has been described to occur extensively between different genotypes within the human HBV lineage, no recombination event has ever been reported between human and non-human primate HBV sequences. It was our objective to perform an exhaustive search for recombination between human and non-human primate HBV strains among all available full-length human and non-human primate HBV sequences, using bootscanning and phylogenetic analyses. Intriguingly, we found that an HBV sequence isolated from a wild born Pan troglodytes schweinfurthii in East Africa-FG-is a recombinant consisting of HBV infecting chimpanzee (ChHBV) and human genotype C. More specifically, in a fragment of approximately 500 nt (positions 551-1050 spanning half of the RT domain of pol, which overlaps with half of the coding region of the small surface protein), FG grouped with HBV genotype C, while in the rest of the genome it grouped with ChHBV sequences. Phylogenetic analyses showed that in the latter region FG was more closely related to the Pan troglodytes troglodytes subspecies, forming an outlier to this group. Moreover, we show evidence that the recombination event occurred after the initial dispersion of HBV genotype C in humans. Finally, our findings point out that although rare recombination between HBV viruses infecting different species occurs
Cellular HIV-1 DNA load predicts HIV-RNA rebound and the outcome of highly active antiretroviral therapy
Objective: To assess whether cellular HIV-1 DNA prior to highly active
antiretroviral therapy (HAART) initiation predicts its outcome.
Design and methods: Patients included all 51 hemophiliacs of the Greek
component of the Multicenter Hemophilia Cohort Study who had initiated
HAART and for whom cryopreserved lymphocyte samples before HAART
initiation were available. Cellular HIV-1 DNA quantification was
performed by a molecular beacon-based real-time PCR assay in multiple
samples per patient with a median (interquartile range) follow-up of 76
(45-102) weeks.
Results: The median (range) baseline HIV-1 DNA load was 297 (< 10 to
3468) copies per 1 x 10(6) peripheral blood mononuclear cells. Baseline
HIV-1 DNA load did not predict initial virological response (VR). None
of the patients with initial VR and baseline HIV-1 DNA load at or below
the median experienced a subsequent virological rebound, while the
cumulative probability of virological rebound by week 104 was 55% among
those with HIV-1 DNA load greater than the median (P<0.008). Cellular
HIV-1 DNA load was the only parameter associated with sustained
virological response as shown by univariate or multivariate analyses
[adjusted odds ratio (95% confidence interval) 0.197 (0.048-0.801)
per 1 log(10) increase in DNA copies, P = 0.023].
Conclusion: Low cellular HIV-1 DNA load is a marker of sustained
virological response in patients with initial VR and it can reliably
predict the long-term success of HAART. (C) 2004 Lippincott Williams
Wilkins
IFN-alpha 2b monotherapy in patients with chronic hepatitis C and persistently normal or near normal aminotransferase activity: A randomized, controlled study
To determine the effect of interferon-alpha2b (IFN-alpha2b) on the
long-term suppression of hepatitis C virus (HCV) RNA in patients with
persistently normal or near normal alanine aminotransferase (ALT)
activity, 76 previously untreated patients with serum HCV RNA and ALT
levels <1.5 times the upper limit of normal (ULN) were randomized to
receive either interferon-alpha 2b (IFN-alpha 2b) 5 MU three times a
week for 24 weeks (n = 37) or no treatment (n = 39). HCV RNA testing was
performed at the end of treatment and after a 6-month follow-up period.
Intention-to-treat analysis showed that HCV RNA was detected
significantly less frequently in treated than in untreated patients, at
the end of both treatment and follow-up (43.2% vs. 7.7%, p < 0.001,
and 21.6% vs. 5.1%, p = 0.033, respectively). Among treated patients,
sustained virologic response was significantly higher in non-1 than in
genotype 1 patients (8 of 26 or 30.8% vs. 0 of 11, p = 0.038).
According to multiple logistic regression, untreated patients had a 13.5
times greater risk to be HCV RNA-positive compared with treated patients
(p = 0.040). ALT levels flared up in 3 treated and 9 untreated patients
(p = 0.07), suggesting that these flare-ups are related to the natural
course of chronic HCV infection rather than to IFN-alpha2b. Thus, such
patients could benefit from an IFN-alpha2b in combination with ribavirin
regimen