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Search Results: 1 - 10 of 149118 matches for " Maciej F. Boni equal contributor "
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Early Pandemic Influenza (2009 H1N1) in Ho Chi Minh City, Vietnam: A Clinical Virological and Epidemiological Analysis
Tran Tinh Hien equal contributor,Maciej F. Boni equal contributor ,Juliet E. Bryant equal contributor,Tran Thuy Ngan equal contributor,Marcel Wolbers,Tran Dang Nguyen,Nguyen Thanh Truong,Nguyen Thi Dung,Do Quang Ha,Vo Minh Hien,Tran Tan Thanh,Le Nguyen Truc Nhu,Le Thi Tam Uyen,Pham Thi Nhien,Nguyen Tran Chinh,Nguyen Van Vinh Chau,Jeremy Farrar,H. Rogier van Doorn equal contributor
PLOS Medicine , 2010, DOI: 10.1371/journal.pmed.1000277
Abstract: Background To date, little is known about the initial spread and response to the 2009 pandemic of novel influenza A (“2009 H1N1”) in tropical countries. Here, we analyse the early progression of the epidemic from 26 May 2009 until the establishment of community transmission in the second half of July 2009 in Ho Chi Minh City (HCMC), Vietnam. In addition, we present detailed systematic viral clearance data on 292 isolated and treated patients and the first three cases of selection of resistant virus during treatment in Vietnam. Methods and Findings Data sources included all available health reports from the Ministry of Health and relevant health authorities as well as clinical and laboratory data from the first confirmed cases isolated at the Hospital for Tropical Diseases in HCMC. Extensive reverse transcription (RT)-PCR diagnostics on serial samples, viral culture, neuraminidase-inhibition testing, and sequencing were performed on a subset of 2009 H1N1 confirmed cases. Virological (PCR status, shedding) and epidemiological (incidence, isolation, discharge) data were combined to reconstruct the initial outbreak and the establishment of community transmission. From 27 April to 24 July 2009, approximately 760,000 passengers who entered HCMC on international flights were screened at the airport by a body temperature scan and symptom questionnaire. Approximately 0.15% of incoming passengers were intercepted, 200 of whom tested positive for 2009 H1N1 by RT-PCR. An additional 121 out of 169 nontravelers tested positive after self-reporting or contact tracing. These 321 patients spent 79% of their PCR-positive days in isolation; 60% of PCR-positive days were spent treated and in isolation. Influenza-like illness was noted in 61% of patients and no patients experienced pneumonia or severe outcomes. Viral clearance times were similar among patient groups with differing time intervals from illness onset to treatment, with estimated median clearance times between 2.6 and 2.8 d post-treatment for illness-to-treatment intervals of 1–4 d, and 2.0 d (95% confidence interval 1.5–2.5) when treatment was started on the first day of illness. Conclusions The patients described here represent a cross-section of infected individuals that were identified by temperature screening and symptom questionnaires at the airport, as well as mildly symptomatic to moderately ill patients who self-reported to hospitals. Data are observational and, although they are suggestive, it is not possible to be certain whether the containment efforts delayed community transmission in Vietnam.
Mathematical Models for a New Era of Malaria Eradication
Maciej F Boni ,Caroline O Buckee,Nicholas J White
PLOS Medicine , 2008, DOI: 10.1371/journal.pmed.0050231
Abstract:
High Guanine and Cytosine Content Increases mRNA Levels in Mammalian Cells
Grzegorz Kudla equal contributor ,Leszek Lipinski equal contributor,Fanny Caffin,Aleksandra Helwak,Maciej Zylicz
PLOS Biology , 2006, DOI: 10.1371/journal.pbio.0040180
Abstract: Mammalian genes are highly heterogeneous with respect to their nucleotide composition, but the functional consequences of this heterogeneity are not clear. In the previous studies, weak positive or negative correlations have been found between the silent-site guanine and cytosine (GC) content and expression of mammalian genes. However, previous studies disregarded differences in the genomic context of genes, which could potentially obscure any correlation between GC content and expression. In the present work, we directly compared the expression of GC-rich and GC-poor genes placed in the context of identical promoters and UTR sequences. We performed transient and stable transfections of mammalian cells with GC-rich and GC-poor versions of Hsp70, green fluorescent protein, and IL2 genes. The GC-rich genes were expressed several-fold to over a 100-fold more efficiently than their GC-poor counterparts. This effect was not due to different translation rates of GC-rich and GC-poor mRNA. On the contrary, the efficient expression of GC-rich genes resulted from their increased steady-state mRNA levels. mRNA degradation rates were not correlated with GC content, suggesting that efficient transcription or mRNA processing is responsible for the high expression of GC-rich genes. We conclude that silent-site GC content correlates with gene expression efficiency in mammalian cells.
Guidelines for Identifying Homologous Recombination Events in Influenza A Virus
Maciej F. Boni,Menno D. de Jong,H. Rogier van Doorn,Edward C. Holmes
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0010434
Abstract: The rapid evolution of influenza viruses occurs both clonally and non-clonally through a variety of genetic mechanisms and selection pressures. The non-clonal evolution of influenza viruses comprises relatively frequent reassortment among gene segments and a more rarely reported process of non-homologous RNA recombination. Homologous RNA recombination within segments has been proposed as a third such mechanism, but to date the evidence for the existence of this process among influenza viruses has been both weak and controversial. As homologous recombination has not yet been demonstrated in the laboratory, supporting evidence, if it exists, may come primarily from patterns of phylogenetic incongruence observed in gene sequence data. Here, we review the necessary criteria related to laboratory procedures and sample handling, bioinformatic analysis, and the known ecology and evolution of influenza viruses that need to be met in order to confirm that a homologous recombination event occurred in the history of a set of sequences. To determine if these criteria have an effect on recombination analysis, we gathered 8307 publicly available full-length sequences of influenza A segments and divided them into those that were sequenced via the National Institutes of Health Influenza Genome Sequencing Project (IGSP) and those that were not. As sample handling and sequencing are executed to a very high standard in the IGSP, these sequences should be less likely to be exposed to contamination by other samples or by laboratory strains, and thus should not exhibit laboratory-generated signals of homologous recombination. Our analysis shows that the IGSP data set contains only two phylogenetically-supported single recombinant sequences and no recombinant clades. In marked contrast, the non-IGSP data show a very large amount of potential recombination. We conclude that the presence of false positive signals in the non-IGSP data is more likely than false negatives in the IGSP data, and that given the evidence to date, homologous recombination seems to play little or no role in the evolution of influenza A viruses.
Clinically immune hosts as a refuge for drug-sensitive malaria parasites
Eili Y Klein, David L Smith, Maciej F Boni, Ramanan Laxminarayan
Malaria Journal , 2008, DOI: 10.1186/1475-2875-7-67
Abstract: The model is constructed as a two-stage susceptible-infected-susceptible (SIS) model of malaria transmission that assumes that individuals build up clinical immunity over a period of years. This immunity reduces the frequency and severity of clinical symptoms, and thus their use of drugs. It also reduces an individual's level of infectiousness, but does not impact the likelihood of becoming infected.Simulations found that with the introduction of resistance into a population, clinical immunity can significantly alter the fitness of the resistant parasite, and thereby impact the ability of the resistant parasite to spread from an initial host by reducing the effective reproductive number of the resistant parasite as transmission intensity increases. At high transmission levels, despite a higher basic reproductive number, R0, the effective reproductive number of the resistant parasite may fall below the reproductive number of the sensitive parasite.These results suggest that high-levels of clinical immunity create a natural ecological refuge for drug-sensitive parasites. This provides an epidemiological rationale for historical patterns of resistance emergence and suggests that future outbreaks of resistance are more likely to occur in low- or unstable-transmission settings. This finding has implications for the design of drug policies and the formulation of malaria control strategies, especially those that lower malaria transmission intensity.Malaria is the leading cause of death in children under five in sub-Saharan Africa [1]. Prompt treatment with effective antimalarial drugs could prevent much of the morbidity and mortality associated with clinical malaria, but the evolution of resistance has diminished the therapeutic efficacy of two previous first-line antimalarials, chloroquine (CQ) and sulphadoxine-pyrimethamine (SP). Historically, it has been suggested that resistance to both CQ and SP emerged from a limited number of de novo selection events in areas of low
No observed effect of homologous recombination on influenza C virus evolution
Guan-Zhu Han, Maciej F Boni, Si-Shen Li
Virology Journal , 2010, DOI: 10.1186/1743-422x-7-227
Abstract: The influenza C virus belongs to the Orthomyxoviridae family and is a common cause of mild upper respiratory tract illness. Seroepidemiological studies indicate that it is widely distributed around the world, but isolated infrequently, and the majority of humans acquire antibodies to the virus early in life [1]. In contrast with influenza A and B viruses, the influenza C virus genome consists of only seven single stranded negative-sense RNA segments, the PB2, PB1, P3, HE, NP, M, and NS segments. Analysis of the full genome sequence of type C influenza viruses suggested that reassortment between two different type C influenza viruses occurs frequently in nature [2,3]. Furthermore, influenza C virus has been suggested to be involved in heterologous RNA recombination events [4].Largely because their RNA is always encapsidated by a ribonucleoprotein complex (RNP), single-stranded negative-sense RNA viruses are generally believed to undergo a low rate of homologous recombination [5]. However, there is increasing evidence of homologous recombination involving negative-strand RNA viruses like Newcastle disease virus [5-8], Zaire Ebola virus [9], measles virus [10], and canine distemper virus [11,12]. Homologous recombination has also been demonstrated in the laboratory for respiratory syncytial virus and hantavirus [13,14]. However, the evidence for homologous recombination in influenza viruses has been sparse and controversial. Gibbs et al. proposed that homologous recombination had occurred in the HA gene of 1918 Spanish flu virus [15]. However, the apparent recombination event described by Gibbs et al. is much more likely the result of a difference in the substitution rate between HA1 and HA2 [16]. Several recent studies provide some new evidence for recombination in influenza A virus [17-19]. In particular, He et al. provide evidence for a clade of three recombinant avian influenza sequences [17], but large-scale analyses have shown that anomalies in the influenza sequ
In vivo susceptibility of Plasmodium falciparum to artesunate in Binh Phuoc Province, Vietnam
Hien Tran,Thuy-Nhien Nguyen,Phu Nguyen,Boni Maciej F
Malaria Journal , 2012, DOI: 10.1186/1475-2875-11-355
Abstract: Background By 2009, there were worrying signs from western Cambodia that parasitological responses to artesunate-containing treatment regimens for uncomplicated Plasmodium falciparum malaria were slower than elsewhere which suggested the emergence of artemisinin resistance. Vietnam shares a long land border with Cambodia with a large number of migrants crossing it on a daily basis. Therefore, there is an urgent need to investigate whether there is any evidence of a change in the parasitological response to the artemisinin derivatives in Vietnam. Methods From August 2010 to May 2011, a randomized controlled clinical trial in uncomplicated falciparum malaria was conducted to compare two doses of artesunate (AS) (2mg/kg/day versus 4 mg/kg/day for three days) followed by dihydroartemisinin-piperaquine (DHA-PPQ) and a control arm of DHA-PPQ. The goal was characterization of the current efficacy of artesunate in southern Vietnam. The primary endpoint of this study was the parasite clearance half-life; secondary endpoints included the parasite reduction ratios at 24 and 48 hours and the parasite clearance time. Results 166 patients were recruited into the study. The median parasite clearance half-lives were 3.54 (AS 2mg/kg), 2.72 (AS 4mg/kg), and 2.98 hours (DHA-PPQ) (p=0.19). The median parasite-reduction ratio at 24 hours was 48 in the AS 2mg/kg group compared with 212 and 113 in the other two groups, respectively (p=0.02). The proportions of patients with a parasite clearance time of >72 hours for AS 2mg/kg, AS 4mg/kg and DHA-PPQ were 27%, 27%, and 22%, respectively. Early treatment failure occurred in two (4%) and late clinical failure occurred in one (2%) of the 55 patients in the AS 2mg/kg group, as compared with none in the other two study arms. The PCR-corrected adequate clinical and parasitological response (APCR) rates in the three groups were 94%, 100%, and 100% (p=0.04). Conclusions This study demonstrated faster P. falciparum parasite clearance in southern Vietnam than in western Cambodia but slower clearance in comparison with historical data from Vietnam. Further studies to determine whether this represents the emergence of artemisinin resistance in this area are needed. Currently, the therapeutic response to DHA-PPQ remains satisfactory in southern Vietnam. Trial registration NTC01165372
U87MG Decoded: The Genomic Sequence of a Cytogenetically Aberrant Human Cancer Cell Line
Michael James Clark equal contributor,Nils Homer equal contributor,Brian D. O'Connor equal contributor,Zugen Chen equal contributor,Ascia Eskin,Hane Lee,Barry Merriman,Stanley F. Nelson
PLOS Genetics , 2010, DOI: 10.1371/journal.pgen.1000832
Abstract: U87MG is a commonly studied grade IV glioma cell line that has been analyzed in at least 1,700 publications over four decades. In order to comprehensively characterize the genome of this cell line and to serve as a model of broad cancer genome sequencing, we have generated greater than 30× genomic sequence coverage using a novel 50-base mate paired strategy with a 1.4kb mean insert library. A total of 1,014,984,286 mate-end and 120,691,623 single-end two-base encoded reads were generated from five slides. All data were aligned using a custom designed tool called BFAST, allowing optimal color space read alignment and accurate identification of DNA variants. The aligned sequence reads and mate-pair information identified 35 interchromosomal translocation events, 1,315 structural variations (>100 bp), 191,743 small (<21 bp) insertions and deletions (indels), and 2,384,470 single nucleotide variations (SNVs). Among these observations, the known homozygous mutation in PTEN was robustly identified, and genes involved in cell adhesion were overrepresented in the mutated gene list. Data were compared to 219,187 heterozygous single nucleotide polymorphisms assayed by Illumina 1M Duo genotyping array to assess accuracy: 93.83% of all SNPs were reliably detected at filtering thresholds that yield greater than 99.99% sequence accuracy. Protein coding sequences were disrupted predominantly in this cancer cell line due to small indels, large deletions, and translocations. In total, 512 genes were homozygously mutated, including 154 by SNVs, 178 by small indels, 145 by large microdeletions, and 35 by interchromosomal translocations to reveal a highly mutated cell line genome. Of the small homozygously mutated variants, 8 SNVs and 99 indels were novel events not present in dbSNP. These data demonstrate that routine generation of broad cancer genome sequence is possible outside of genome centers. The sequence analysis of U87MG provides an unparalleled level of mutational resolution compared to any cell line to date.
Nipbl and Mediator Cooperatively Regulate Gene Expression to Control Limb Development
Akihiko Muto,Shingo Ikeda,Martha E. Lopez-Burks,Yutaka Kikuchi equal contributor,Anne L. Calof equal contributor ,Arthur D. Lander equal contributor ,Thomas F. Schilling equal contributor
PLOS Genetics , 2014, DOI: doi/10.1371/journal.pgen.1004671
Abstract: Haploinsufficiency for Nipbl, a cohesin loading protein, causes Cornelia de Lange Syndrome (CdLS), the most common “cohesinopathy”. It has been proposed that the effects of Nipbl-haploinsufficiency result from disruption of long-range communication between DNA elements. Here we use zebrafish and mouse models of CdLS to examine how transcriptional changes caused by Nipbl deficiency give rise to limb defects, a common condition in individuals with CdLS. In the zebrafish pectoral fin (forelimb), knockdown of Nipbl expression led to size reductions and patterning defects that were preceded by dysregulated expression of key early limb development genes, including fgfs, shha, hand2 and multiple hox genes. In limb buds of Nipbl-haploinsufficient mice, transcriptome analysis revealed many similar gene expression changes, as well as altered expression of additional classes of genes that play roles in limb development. In both species, the pattern of dysregulation of hox-gene expression depended on genomic location within the Hox clusters. In view of studies suggesting that Nipbl colocalizes with the mediator complex, which facilitates enhancer-promoter communication, we also examined zebrafish deficient for the Med12 Mediator subunit, and found they resembled Nipbl-deficient fish in both morphology and gene expression. Moreover, combined partial reduction of both Nipbl and Med12 had a strongly synergistic effect, consistent with both molecules acting in a common pathway. In addition, three-dimensional fluorescent in situ hybridization revealed that Nipbl and Med12 are required to bring regions containing long-range enhancers into close proximity with the zebrafish hoxda cluster. These data demonstrate a crucial role for Nipbl in limb development, and support the view that its actions on multiple gene pathways result from its influence, together with Mediator, on regulation of long-range chromosomal interactions.
Crossing the Line: Selection and Evolution of Virulence Traits
Nat F Brown equal contributor,Mark E Wickham equal contributor,Brian K Coombes,B. Brett Finlay
PLOS Pathogens , 2006, DOI: 10.1371/journal.ppat.0020042
Abstract: The evolution of pathogens presents a paradox. Pathogenic species are often absolutely dependent on their host species for their propagation through evolutionary time, yet the pathogenic lifestyle requires that the host be damaged during this dependence. It is clear that pathogenic strategies are successful in evolutionary terms because a diverse array of pathogens exists in nature. Pathogens also evolve using a broad range of molecular mechanisms to acquire and modulate existing virulence traits in order to achieve this success. Detailing the benefit of enhanced selection derived through virulence and understanding the mechanisms through which virulence evolves are important to understanding the natural world and both have implications for human health.
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