323 research outputs found

    Detection of the spotted wing drosophila, Drosophila suzukii, in continental sub-Saharan Africa

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    The spotted wing drosophila, Drosophila suzukii Matsumura, is an insect pest of soft-skinned fruit, native to Eastern Asia. Since 2008, a world-wide dispersal of D. suzukii is seen, characterized by the establishment of the pest in many Asian, American and European countries. While the potential for invasion of continental Africa by D. suzukii has been predicted, its presence has only been shown for Morocco in Northern Africa. Knowledge about a possible establishment in other parts of the continent is needed as a basis for pest management. In 2019, we carried out a first survey in three counties in Kenya to monitor for the presence of D. suzukii using traps baited with a blend of apple cider vinegar and red wine. A total of 389 D. suzukii flies were captured in a fruit farm at Nakuru county, with more female flies being trapped than males. We confirmed the morphological identification of D. suzukii using DNA barcoding. In 2020, we performed a follow-up survey at 14 locations in six counties to delimit the distribution of D. suzukii in the main berry growing zones in Kenya. The survey indicated that so far D. suzukii is restricted to Nakuru county where it was initially detected. This is the first study to provide empirical evidence of D. suzukii in continental sub-Saharan Africa, confirming that the pest is expanding its geographic range intercontinentally. Given the high dispersal potential of D. suzukii, a concerted effort to develop management strategies is a necessity for containment of the pest

    Communications Biophysics

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    Contains research objectives, summary of research and reports on three research projects.National Institutes of Health (Grant 5 PO1 GM14940-06)National Institutes of Health (Grant 2 TOl GM01555-06)National Institutes of Health (Grant 1 ROl NS10737-01)National Aeronautics and Space Administration (Grant NGL 22-009-304)Joint Services Electronics Programs (U. S. Army, U. S. Navy, and U. S. Air Force) under Contract DAAB07-71-C-0300B-D Electrodyne Division, Becton Dickinson and Company (Grant)Boston City Hospital Purchase Order 1176-21-33

    A Study of B0 -> J/psi K(*)0 pi+ pi- Decays with the Collider Detector at Fermilab

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    We report a study of the decays B0 -> J/psi K(*)0 pi+ pi-, which involve the creation of a u u-bar or d d-bar quark pair in addition to a b-bar -> c-bar(c s-bar) decay. The data sample consists of 110 1/pb of p p-bar collisions at sqrt{s} = 1.8 TeV collected by the CDF detector at the Fermilab Tevatron collider during 1992-1995. We measure the branching ratios to be BR(B0 -> J/psi K*0 pi+ pi-) = (8.0 +- 2.2 +- 1.5) * 10^{-4} and BR(B0 -> J/psi K0 pi+ pi-) = (1.1 +- 0.4 +- 0.2) * 10^{-3}. Contributions to these decays are seen from psi(2S) K(*)0, J/psi K0 rho0, J/psi K*+ pi-, and J/psi K1(1270)

    Diffractive Dijet Production at sqrt(s)=630 and 1800 GeV at the Fermilab Tevatron

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    We report a measurement of the diffractive structure function FjjDF_{jj}^D of the antiproton obtained from a study of dijet events produced in association with a leading antiproton in pˉp\bar pp collisions at s=630\sqrt s=630 GeV at the Fermilab Tevatron. The ratio of FjjDF_{jj}^D at s=630\sqrt s=630 GeV to FjjDF_{jj}^D obtained from a similar measurement at s=1800\sqrt s=1800 GeV is compared with expectations from QCD factorization and with theoretical predictions. We also report a measurement of the ξ\xi (xx-Pomeron) and β\beta (xx of parton in Pomeron) dependence of FjjDF_{jj}^D at s=1800\sqrt s=1800 GeV. In the region 0.035<ξ<0.0950.035<\xi<0.095, t<1|t|<1 GeV2^2 and β<0.5\beta<0.5, FjjD(β,ξ)F_{jj}^D(\beta,\xi) is found to be of the form β1.0±0.1ξ0.9±0.1\beta^{-1.0\pm 0.1} \xi^{-0.9\pm 0.1}, which obeys β\beta-ξ\xi factorization.Comment: LaTeX, 9 pages, Submitted to Phys. Rev. Letter

    Real-time imaging of hepatitis C virus infection using a fluorescent cell-based reporter system

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    Author Manuscript 2010 August 1Hepatitis C virus (HCV), which infects 2–3% of the world population, is a causative agent of chronic hepatitis and the leading indication for liver transplantation1. The ability to propagate HCV in cell culture (HCVcc) is a relatively recent breakthrough and a key tool in the quest for specific antiviral therapeutics. Monitoring HCV infection in culture generally involves bulk population assays, use of genetically modified viruses and/or terminal processing of potentially precious samples. Here we develop a cell-based fluorescent reporter system that allows sensitive distinction of individual HCV-infected cells in live or fixed samples. We demonstrate use of this technology for several previously intractable applications, including live-cell imaging of viral propagation and host response, as well as visualizing infection of primary hepatocyte cultures. Integration of this reporter with modern image-based analysis methods could open new doors for HCV research.New York (State). Dept. of Health (Empire State Stem Cell Fund Contract C023046)United States. Public Health Service (Grant R01 DK56966)National Institutes of Health (U.S.) (Roadmap for Medical Research Grant 1 R01 DK085713-01)Howard Hughes Medical Institute (Investigator

    Communications Biophysics

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    Contains research objectives and summary of research on thirteen research projects split into four section.National Institutes of Health (Grant 1 RO1 NS10737-01)National Institutes of Health (Grant 1 ROI NS10916-01)National Institutes of Health (Grant 5 RO1 NS11000-02)National Institutes of Health (Grant 1 RO1 NS11153-01)Harvard M.I.T. Rehabilitation Engineering CenterU. S. Department of Health, Education, and Welfare, Grant 23-P-55854National Institutes of Health (Grant 1 RO1 NS11680-01)Norlin Music, Inc.Clarence J. LeBel FundNational Institutes of Health (Grant 1 RO1 NS11080-01A1)National Institutes of Health (Grant 5 TO1 GM01555-08)M.I.T. Health Sciences FundBoston City Hospital Purchase Order 1176-05-21335-C

    The Disulfide Bonds in Glycoprotein E2 of Hepatitis C Virus Reveal the Tertiary Organization of the Molecule

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    Hepatitis C virus (HCV), a major cause of chronic liver disease in humans, is the focus of intense research efforts worldwide. Yet structural data on the viral envelope glycoproteins E1 and E2 are scarce, in spite of their essential role in the viral life cycle. To obtain more information, we developed an efficient production system of recombinant E2 ectodomain (E2e), truncated immediately upstream its trans-membrane (TM) region, using Drosophila melanogaster cells. This system yields a majority of monomeric protein, which can be readily separated chromatographically from contaminating disulfide-linked aggregates. The isolated monomeric E2e reacts with a number of conformation-sensitive monoclonal antibodies, binds the soluble CD81 large external loop and efficiently inhibits infection of Huh7.5 cells by infectious HCV particles (HCVcc) in a dose-dependent manner, suggesting that it adopts a native conformation. These properties of E2e led us to experimentally determine the connectivity of its 9 disulfide bonds, which are strictly conserved across HCV genotypes. Furthermore, circular dichroism combined with infrared spectroscopy analyses revealed the secondary structure contents of E2e, indicating in particular about 28% β-sheet, in agreement with the consensus secondary structure predictions. The disulfide connectivity pattern, together with data on the CD81 binding site and reported E2 deletion mutants, enabled the threading of the E2e polypeptide chain onto the structural template of class II fusion proteins of related flavi- and alphaviruses. The resulting model of the tertiary organization of E2 gives key information on the antigenicity determinants of the virus, maps the receptor binding site to the interface of domains I and III, and provides insight into the nature of a putative fusogenic conformational change

    A Novel Small Molecule Inhibitor of Hepatitis C Virus Entry

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    Small molecule inhibitors of hepatitis C virus (HCV) are being developed to complement or replace treatments with pegylated interferons and ribavirin, which have poor response rates and significant side effects. Resistance to these inhibitors emerges rapidly in the clinic, suggesting that successful therapy will involve combination therapy with multiple inhibitors of different targets. The entry process of HCV into hepatocytes represents another series of potential targets for therapeutic intervention, involving viral structural proteins that have not been extensively explored due to experimental limitations. To discover HCV entry inhibitors, we utilized HCV pseudoparticles (HCVpp) incorporating E1-E2 envelope proteins from a genotype 1b clinical isolate. Screening of a small molecule library identified a potent HCV-specific triazine inhibitor, EI-1. A series of HCVpp with E1-E2 sequences from various HCV isolates was used to show activity against all genotype 1a and 1b HCVpp tested, with median EC50 values of 0.134 and 0.027 µM, respectively. Time-of-addition experiments demonstrated a block in HCVpp entry, downstream of initial attachment to the cell surface, and prior to or concomitant with bafilomycin inhibition of endosomal acidification. EI-1 was equally active against cell-culture adapted HCV (HCVcc), blocking both cell-free entry and cell-to-cell transmission of virus. HCVcc with high-level resistance to EI-1 was selected by sequential passage in the presence of inhibitor, and resistance was shown to be conferred by changes to residue 719 in the carboxy-terminal transmembrane anchor region of E2, implicating this envelope protein in EI-1 susceptibility. Combinations of EI-1 with interferon, or inhibitors of NS3 or NS5A, resulted in additive to synergistic activity. These results suggest that inhibitors of HCV entry could be added to replication inhibitors and interferons already in development
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