Retroactive News.2017

Total Page:16

File Type:pdf, Size:1020Kb

Retroactive News.2017 Newsletter of the Center for Retrovirus Research at The Ohio State University 2017 Highlights Dr. Li Wu awarded NIH R01 to study how RNA modifications modulate retroviral infection Dr. Li Wu has been awarded a replication in CD4+ T-cells by affecting the structure, new $1.42 million R01 grant from stability, splicing, and/or trafficking of HIV-1 RNA. NIH to investigate how HIV-1 Investigations of the HIV-1 RNA m6A modification and RNA modifications modulate viral interactions with host proteins represent a new area infection. of HIV-1 RNA biology which can potentially facilitate In this project, Dr. Wu and his therapeutic development against HIV-1 infection. collaborators will study the Dr. Wu’s collaborators in this project include Dr. Chuan molecular mechanisms by which He at University of Chicago and Howard Hughes Medical 6 6 N -methyladenosine (m A) Institute, Drs. Karin Musier-Forsyth and Mark Foster at modification of HIV-1 RNA regulates The Ohio State University, and Dr. Mamuka Kvaratskhelia viral replication in CD4+ T-cells. They hypothesize that at the University of Colorado. reversible m6A modification of HIV-1 RNA regulates viral Dr. Namal Liyanage, PhD joins the Ohio State faculty and the CRR Dr. Namal Liyanage was recruited during the ALVAC-SIV prime boost vaccination strategy to join the Departments of Microbial in collaboration with Dr. Rafick-Pierre Sekaly, at Case Infection and Immunity and Western Reserve University. Veterinary Biosciences, and the Dr. Liyanage is the recipient of a 2016 NIH career Center for Retrovirus Research transition grant (K22 Award). Dr. Liyanage’s lab at Ohio (CRR), as part of the university’s State mainly focuses on understanding the role of the Discovery Themes initiative. innate and adaptive immune systems during chronic Dr. Liyanage received his viral infections and development of novel strategies to postdoctoral training with Dr. Genoveffa Franchini at prevent and control chronic viral infections, such as HIV. the NIH, followed by a research fellow position in the His lab currently is conducting studies to understand laboratory of Immune Biology and Retroviral section the role of NK/ILCs and innate memory in the RV144 HIV under Dr. Marjorie Robert-Guroff in the Vaccine Branch vaccine strategy, exploring the regulatory role of NK/ILCs at NCI. During his post-doctoral training, Dr. Liyanage on B and T cells during vaccines and discovery of novel studied the role of NK and mucosal innate lymphoid cells adjuvants that enhance HIV vaccine efficacy. (ILCs) in HIV/SIV pathogenesis and vaccines. His laboratory is also conducting research on Dr. Liyanage was a member of the team that understanding the immunopathology of HIV/TB, HIV/ recapitulated the RV144 clinical trial, the first human HCV and HIV/Zika co-infections and Dengue infection vaccine trial to show limited but significant protection by collaborating with several national and international from HIV acquisition in rhesus macaques. In a separate academic and industrial partners. Welcome Namal! study, he investigated the innate gene regulation vet.osu.edu/retrovirus-research 1 Dr. Li Wu was elected fellow of the American Association for the Advancement of Science (AAAS) Center member, Dr. Li Wu, Professor in the Department of the honor of Fellow in recognition of their scientific Veterinary Biosciences, has been elected as a Fellow of or socially distinguished efforts to advance science the AAAS for his distinguished contributions to the field or its applications. Four Ohio State faculty members of molecular virology, particularly for the mechanisms of were among 396 AAAS members who received the HIV replication and the virus interactions with host cells. prestigious honor this year. vet.osu.edu/about-us/news/ Election as an AAAS Fellow is a prestigious honor dr-wu-receives-prestigious-science-honor bestowed upon AAAS members by their peers. New Other Center Members that are AAAS Fellows include; fellows will be presented with an official certificate and Patrick Green, Karin Musier-Forsyth, Michael Oglesbee, a gold and blue rosette pin at the 2018 AAAS Annual Christopher Walker, and Caroline Whitacre. Meeting in Austin, TX in February 2018. Members receive Miguel Lopez selected for prestigious career development opportunity Miguel A. Lopez Jr., a PhD engagement and participation of people from diverse graduate student in Dr. Kristine backgrounds. Yoder’s lab, has been accepted The program includes several components that to the Yale Ciencia Academy are designed to train participants to be successful, (YCA) 2018 career development productive and culturally conscientious scientists. cohort. He is one of only 40 Training culminates with a capstone project where doctoral students nationwide students lead science outreach initiatives in their own selected. communities. This opportunity will allow Miguel to The YCA is a year-long NIH develop as a scientist and learn how to further aid other funded program aimed minority scientists to thrive here at Ohio State. to develop traditionally Miguel is looking forward to making the most of this underrepresented graduate exciting opportunity. Good luck Miguel! students through direct mentoring, peer support and networking. It utilizes STEM networks to enhance the Dr. Shan-Lu Liu named as Co-Director of the Viruses and Emerging Pathogens Program of The Ohio State University’s Infectious Diseases Institute (IDI) Dr. Shan-Lu Liu, a center in this program collaborate with campus, regional, investigator and Professor of national and international colleagues and leaders to the Departments of Veterinary better understand the etiology, transmission, immunity Biosciences, Microbiology, and and pathogenesis of viruses and emerging pathogens, Microbial Infection and Immunity with an ultimate goal of developing innovative and has been selected, along with highly effective strategies for diagnosis, prevention and Dr. Linda Saif, as Co-Director treatment. of the Viruses and Emerging VEP scientists actively work on HIV, HTLV, coronaviruses Pathogens Program (VEP) of the (PEDV, MERS, SARS), Ebola virus, noroviruses, Ohio State IDI. rotaviruses, hepatitis viruses, Zika virus, influenza The IDI was established by the viruses, sea viruses, and more, as well as on animal university in 2017 in order to and plant pathogens that are possible sources of accelerate infectious disease research and education transmission to humans. The research topics in this across campuses. VEP is one of the six thematic program cover the basic virology, immunity, microbiome, programs within the institute, the mission of which is to nutrition, pathogenesis, diagnosis, animal models, facilitate research, training and educational outreach vaccine development, treatment, and more. focused on viruses and emerging pathogens. Scientists Retro-Active News - 2017 Highlights vet.osu.edu/retrovirus-research 2 Dr. Kristine Yoder awarded NIH R01 to investigate the mechanics of retroviral integration in real-time. Dr. Kristine Yoder, Assistant integration analysis, and novel single molecule imaging Professor, Department of techniques to visualize the retroviral integration process Cancer Biology and Genetics in real-time. and member of the Center The specific aims are to 1) detail the target site selection for Retrovirus Research, has process of the PFV intasome, 2) examine the dynamics of received a five-year multi-PI (R. retroviral IN protein and viral cDNA following integration, Fishel) grant of $1.95M from the and 3) determine the influence of defined chromatin on National Institutes of Health. retroviral intasome dynamics and target site selection. Dr. Yoder is utilizing the non- These studies are designed to interrogate the animated pathogenic prototype foamy processes associated with PFV integration to provide a virus (PFV), an unsurpassed quantitative biophysical foundation for retroviral intasome biophysical model for retrovirus progressions. Drs. Musier-Forsyth and Kvaratskhelia receive funding as part of the NIH U54 Collaborative HIV Interaction in Viral Evolution (HIVE) Center The HIVE Center, which To accomplish this goal, the program will explore the was recently renewed structural and biophysical interactions of HIV Gag and for a second 5-year term, Gag-Pol polyproteins, capsid, reverse transcriptase, and comprises a group of highly integrase and their evolutionary relationships. collaborative investigators The Center’s research focus also extends to cellular with deep experience in HIV factors that inform the structural and macromolecular research and well established dynamics of events in reverse transcription, assembly, expertise in structural, and integration and includes studies on how APOBEC3 biophysical, biochemical, and proteins suppress reverse transcription, and the role of computational biology, as well LEDGF in guiding viral integration and its contribution to as synthetic chemistry, and latency in conjunction with CPSF6. virology. The Center is aimed at understanding the system The HIVE Center is directed by Drs. Stefan Sarafianos interdependency of interacting HIV macromolecules and (Emory University) and Bruce Torbett (The Scripps their assemblies, which shape the HIV life cycle. Research Institute). www.scripps.edu/hive_center/index.html Congratulations! Professor Mamuka Kvarastkhelia departed Ohio State in August, 2017 to join the University of Colorado School of Medicine, Division of Infectious Diseases. Congratulations Mamuka and we wish you the best in your new position. Retro-Active News - 2017 Highlights
Recommended publications
  • Chain Maturation and Surface Expression Heavy Μ and D Μ
    Conventional and Surrogate Light Chains Differentially Regulate Ig µ and Dµ Heavy Chain Maturation and Surface Expression This information is current as Terry Fang, Brendan P. Smith and Christopher A. J. Roman of October 5, 2021. J Immunol 2001; 167:3846-3857; ; doi: 10.4049/jimmunol.167.7.3846 http://www.jimmunol.org/content/167/7/3846 Downloaded from References This article cites 73 articles, 34 of which you can access for free at: http://www.jimmunol.org/content/167/7/3846.full#ref-list-1 Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on October 5, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2001 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Conventional and Surrogate Light Chains Differentially Regulate Ig ␮ and D␮ Heavy Chain Maturation and Surface Expression1 Terry Fang, Brendan P. Smith, and Christopher A. J. Roman2 Positive selection of precursor (pre-) B cells by Ig membrane ␮ H chains (␮m HC) and counterselection mediated by the truncated HC D␮ depend on the ability of each HC to form a pre-B cell receptor (pre-BCR) signaling complex with the surrogate L chain (SLC) components ␭5 and Vpre-B.
    [Show full text]
  • Genome-Wide Rnai Screen Identifies Broadly-Acting Host Factors That Inhibit Arbovirus Infection." Plos Pathogens.10,2
    Washington University School of Medicine Digital Commons@Becker Open Access Publications 2014 Genome-wide RNAi screen identifies broadly- acting host factors that inhibit arbovirus infection Ari Yasunaga University of Pennsylvania Sheri L. Hanna University of Pennsylvania Jianqing Li Washington University School of Medicine in St. Louis Hyelim Cho Washington University School of Medicine in St. Louis Patrick P. Rose University of Pennsylvania See next page for additional authors Follow this and additional works at: https://digitalcommons.wustl.edu/open_access_pubs Recommended Citation Yasunaga, Ari; Hanna, Sheri L.; Li, Jianqing; Cho, Hyelim; Rose, Patrick P.; Spiridigliozzi, Anna; Gold, Beth; Diamond, Michael S.; and Cherry, Sara, ,"Genome-wide RNAi screen identifies broadly-acting host factors that inhibit arbovirus infection." PLoS Pathogens.10,2. e1003914. (2014). https://digitalcommons.wustl.edu/open_access_pubs/2700 This Open Access Publication is brought to you for free and open access by Digital Commons@Becker. It has been accepted for inclusion in Open Access Publications by an authorized administrator of Digital Commons@Becker. For more information, please contact [email protected]. Authors Ari Yasunaga, Sheri L. Hanna, Jianqing Li, Hyelim Cho, Patrick P. Rose, Anna Spiridigliozzi, Beth Gold, Michael S. Diamond, and Sara Cherry This open access publication is available at Digital Commons@Becker: https://digitalcommons.wustl.edu/open_access_pubs/2700 Genome-Wide RNAi Screen Identifies Broadly-Acting Host Factors That Inhibit
    [Show full text]
  • Forty Years with Coronaviruses
    VIEWPOINT Forty years with coronaviruses Susan R. Weiss I have been researching coronaviruses for more than forty years. This viewpoint summarizes some of the major findings in coronavirus research made before the SARS epidemic and how they inform current research on the newly emerged SARS-CoV-2. A virulent new coronavirus is currently didn’t want to continue working in that including infectious bronchitis virus and bo- holding hostage much of the human popu- field. In reading the literature, I came upon vine coronavirus. There were a handful of Downloaded from https://rupress.org/jem/article-pdf/217/5/e20200537/1041300/jem_20200537.pdf by guest on 30 March 2020 lation worldwide. This virus, SARS-CoV-2, coronaviruses as an attractive topic, with presentations on human coronavirus 229E, a which causes the COVID-19 disease, so much possible. The model coronavirus, poorly understood agent of the common cold. emerged in China from bats into a presumed mouse hepatitis virus (MHV), was easy to Leaving that meeting, and with the en- intermediate species and then into humans. grow in tissue culture in the laboratory and couragement and mentorship of Neal It then spread around the globe with ongo- also provided compelling mouse models for Nathanson, my chair, and Don Gilden, a ing devastating effects. This round of human human disease, especially those of the liver professor in the neurology department, I coronavirus disease follows the appearance and the central nervous system. Julian Lei- was excited to expand my research to of the related lethal coronaviruses, SARS- bowitz, then at the University of California, studies utilizing the MHV animal models of CoV and MERS-CoV, in 2002 and 2012 re- San Diego, working on MHV, very gener- both encephalitis/chronic demyelinating spectively.
    [Show full text]
  • Download Program
    Oral Program Sunday, October 1, 2017 11:00-13:00 Registration Room: Hotel Lobby North/Assembly Foyer Room South Ballroom 13:00-13:15 Opening Remarks, Editorial Organizers 13:15-14:15 Opening Keynote: Anthony S. Fauci, NIAID, USA Emerging and Re-Emerging Infectious Diseases: From AIDS to Zika [KEY1] 14:15-17:45 Session 1: Genomics & Evolution Session Chair: Akiko Iwasaki, Yale University 14:15-14:45 George Fu Gao, Chinese Academy of Sciences, China Enveloped virus entry: From Flu to Ebola [INV01] 14:45-15:00 [ST01] Functional Evolution of Zika Virus in the Americas N.D. Grubaugh*, C. Ontiveros, R. Agarwal, T. Rogers, N. Beutler, K. Gangavarapu, G. Oliveira, R. Robles- Sikisaka, D. Burton, K.G. Andersen The Scripps Research Institute, USA 15:00-15:15 [ST02] Characterization of a clade-defining Ebola virus glycoprotein mutant from the 2013-2016 epidemic W.E. Diehl1, D. Mu1, A.E. Lin3, M. Cabot2, K.G. Andersen4, J.H. Kuhn6, P. Sabeti3, B. Ganser-Pornillos2, J. White2, J. Luban*1 et al 1University of Massachusetts Medical School, USA, 2University of Virginia, USA, 3Harvard University, USA, 4The Scripps Research Institute, USA, 5University of Edinburgh, UK, 6NIAID, USA 15:15-15:45 Gustavo Palacios, USAMRIID Center for Genomic Sciences, USA Near real-time genomics applications in clinical virology and biosurveillance [INV02] 15:45-16:15 Refreshment Break Room: North Ballroom 16:15-16:45 Linfa Wang, Duke-NUS Medical School, Singapore Programme in emerging infectious diseases [INV03] 16:45-17:00 [ST03] Immune correlates of protection from a universal influenza vaccine during intra- and intersubtypic heterologous challenge with H1, H6, H7 and H10 influenza viruses J.C.
    [Show full text]
  • Virus Recognition by Toll-7 Activates Antiviral Autophagy in Drosophila
    Immunity Article Virus Recognition by Toll-7 Activates Antiviral Autophagy in Drosophila Margaret Nakamoto,1,2 Ryan H. Moy,1,2 Jie Xu,1 Shelly Bambina,1 Ari Yasunaga,1 Spencer S. Shelly,1 Beth Gold,1 and Sara Cherry1,* 1Department of Microbiology, Penn Genome Frontiers Institute, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA 2These authors contributed equally to this work *Correspondence: [email protected] DOI 10.1016/j.immuni.2012.03.003 SUMMARY tion molecules that activate a proteolytic cascade converging on the activation of spa¨ tzle, a cytokine that binds to Toll thereby Innate immunity is highly conserved and relies on inducing an NF-kB-dependent transcriptional program for anti- pattern recognition receptors (PRRs) such as Toll- microbial defense. Surprisingly, a role for the additional eight like receptors (identified through their homology to Drosophila Toll homologs in innate immune defense has yet to Drosophila Toll) for pathogen recognition. Although be established. Toll-2 (18-wheeler) may have a minor role in Drosophila Toll is vital for immune recognition and the antibacterial response (Ligoxygakis et al., 2002; Williams defense, roles for the other eight Drosophila Tolls in et al., 1997), and Toll-5 (Tehao) and Toll-9 can activate the expression of the antifungal gene Drosomycin (Bilak et al., immunity have remained elusive. Here we have 2003; Luo et al., 2001; Ooi et al., 2002; Tauszig et al., 2000). shown that Toll-7 is a PRR both in vitro and in adult However, these receptors have not been implicated as essential flies; loss of Toll-7 led to increased vesicular stoma- components of the immune response or in the recognition of any titis virus (VSV) replication and mortality.
    [Show full text]
  • Endocytosis of Mosquito-Borne Flaviviruses
    viruses Review Beyond the Surface: Endocytosis of Mosquito-Borne Flaviviruses Stephen D. Carro and Sara Cherry * Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA; [email protected] * Correspondence: [email protected] Abstract: Flaviviruses are a group of positive-sense RNA viruses that are primarily transmitted through arthropod vectors and are capable of causing a broad spectrum of diseases. Many of the flaviviruses that are pathogenic in humans are transmitted specifically through mosquito vectors. Over the past century, many mosquito-borne flavivirus infections have emerged and re-emerged, and are of global importance with hundreds of millions of infections occurring yearly. There is a need for novel, effective, and accessible vaccines and antivirals capable of inhibiting flavivirus infection and ameliorating disease. The development of therapeutics targeting viral entry has long been a goal of antiviral research, but most efforts are hindered by the lack of broad-spectrum potency or toxicities associated with on-target effects, since many host proteins necessary for viral entry are also essential for host cell biology. Mosquito-borne flaviviruses generally enter cells by clathrin-mediated endocytosis (CME), and recent studies suggest that a subset of these viruses can be internalized through a specialized form of CME that has additional dependencies distinct from canonical CME pathways, and antivirals targeting this pathway have been discovered. In this review, we discuss the role and contribution of endocytosis to mosquito-borne flavivirus entry as well as consider past and future efforts to target endocytosis for therapeutic interventions. Keywords: flavivirus; mosquito-borne; clathrin-mediated; endocytosis; receptors; RNASEK; LY6E; Citation: Carro, S.D.; Cherry, S.
    [Show full text]
  • Influence of Herd Immunity in the Cyclical Nature of Arboviruses
    Available online at www.sciencedirect.com ScienceDirect Influence of herd immunity in the cyclical nature of arboviruses 1,2 3 4 Guilherme S Ribeiro , Gabriel L Hamer , Mawlouth Diallo , 5 6 7 Uriel Kitron , Albert I Ko and Scott C Weaver We review and contrast the evidence for an effect of amplifying Introduction to arboviruses and their host herd immunity on circulation and human exposure to transmission arboviruses. Herd immunity of short-lived West Nile virus avian Arthropod-borne viruses (arboviruses) are transmitted amplifying hosts appears to play a limited role in levels of biologically, involving replication in arthropod vectors enzootic circulation and spillover infections of humans, which and vertebrate amplifying hosts [1]. The development are not amplifiers. In contrast, herd immunity of nonhuman of adaptive immunity, if it prevents secondary infection primate hosts for enzootic Zika, dengue, and chikungunya and viremia, removes hosts from the pool of susceptible viruses is much stronger and appears to regulate to a large amplifiers. Herd immunity can therefore have major extent the periodicity of sylvatic amplification in Africa. impacts on arbovirus circulation and disease, and Following the recent Zika and chikungunya pandemics, human the temporality and cycling of epidemic and endemic herd immunity in the Americas quickly rose to 50% in many transmission [2]. regions, although seroprevalence remains patchy. Modeling from decades of chikungunya circulation in Asia suggests that All arboviruses originated as zoonotic agents that rely on this level of herd immunity will suppress for many years major nonhuman animals as amplifying hosts by generating chikungunya and Zika epidemics in the Americas, followed by viremia needed for oral infection of the vector (Figure 1).
    [Show full text]
  • JEM Goes Viral
    EDITORIAL JEM goes viral Carl F. Nathan1, Michel C. Nussenzweig1, and Teodoro Pulvirenti2 Viral pathogens continue to put people’s lives at risk, from Ebola and Biophysics, Scientific Director of the High-throughput to Zika, dengue, Chikungunya, influenza, HIV, and more. While Screening Core, and Director of the Chemogenomic Discov- prominent progress has been made to treat HIV infection and ery Program in the School of Medicine at the University of reduce its spread, HIV and many other viruses, including in- Pennsylvania. She obtained her BS with Dr. Peter Schultz at fluenza, remain a major menace. In the midst of the search for Berkeley synthesizing new biopolymers for drug scaffolds, new vaccines (see Rappuoli et al. 2019. J. Exp. Med. https://doi. and then her PhD with Dr. David Baltimore at MIT studying org/10.1084/jem.20182160) and treatments and faced with early B cell development. Dr. Cherry completed her post- counterproductive anti-vaccination movements, we believe it is doctoral fellowship with Dr. Norbert Perrimon, with whom more important than ever for JEM to emphasize the journal’s she developed high-throughput RNAi screening to study interest in studies related to viral infection and to microbiology virus–host interactions. She started her laboratory at Penn in general. With this intention, we welcome Sara Cherry to the in 2006, where she has applied cell-based screening ap- JEM editorial board. proaches to discover mechanisms by which diverse viral Sara Cherry is a Professor in the Department of Pathology pathogens hijack cellular machinery while evading innate and Laboratory Medicine and the Department of Biochemistry immune defenses.
    [Show full text]
  • SARS-COV-2 Antiviral Therapeutics Summit Report, November 2020
    SARS-COV-2 ANTIVIRAL THERAPEUTICS SUMMIT REPORT Summit sponsored by the National Institute of Allergy and Infectious Diseases and the National Center for Advancing Translational Sciences NOVEMBER 6, 2020 National Institutes of Health Summit Report Authors Annaliesa Anderson, Pfzer James M. Anderson, Offce of the Director, NIH Kara Carter, Evotec* Tomas Cihlar, Gilead Sciences Anthony J. Conley, National Institute of Allergy and Infectious Diseases, NIH Mindy I. Davis, National Institute of Allergy and Infectious Diseases, NIH Mark Denison, Vanderbilt University Matthew D. Hall, National Center for Advancing Translational Sciences, NIH Daria Hazuda, Merck & Co. Stephanie Moore, University of Alabama at Birmingham George Painter, Emory University Pei-Yong Shi, University of Texas Medical Branch Richard Whitley, University of Alabama at Birmingham *Current affliation: Dewpoint Therapeutics -2- Summit Hosts Dr. Francis Collins, Director, National Institutes of Health (NIH) Dr. Anthony Fauci, Director, National Institute of Allergy and Infectious Diseases (NIAID) Dr. Christopher Austin, Director, National Center for Advancing Translational Sciences (NCATS) Summit Organizers James M. Anderson, Offce of the Director, NIH Kyle R. Brimacombe, NCATS, NIH Anthony J. Conley, NIAID, NIH Mindy I. Davis, NIAID, NIH Stephanie Ford-Scheimer, NCATS, NIH Abigail Grossman, NCATS, NIH Matthew D. Hall, NCATS, NIH -3- TABLE OF CONTENTS Introduction 5 Overview of the Virus and Therapeutics Approaches 7 Viral Replication Machinery 11 Proteases (Viral and Host) 18 Emerging Targets, Emerging Modalities 25 Preclinical Tools 28 Lessons from Other Viruses and Preparation for the Future 33 Summary of Discussions and Perspectives on the Challenges Ahead 38 Resources 43 References 47 -4- INTRODUCTION NIH SARS-COV-2 ANTIVIRAL THERAPEUTICS SUMMIT Presenters: Dr.
    [Show full text]
  • From the President's Desk
    JAN - FEB 2008 From the President’s desk: The Urbilateria Book Project Genetics is thriving as never before, spawning in recent years sub- disciplines such as genomics, bioinformatics, evo-devo, systems biology, and more. If genetics were a business, there would be much talk about its growing market share both in basic science, its traditional realm, and increasingly throughout the world of medicine (with significant upside potential). The ageless questions – how genomes evolved on Earth, how genotype programs phenotype, what makes each of us human but unique, how genetic knowledge can better our lives – suddenly seem less daunting, more like practical tasks. Unsurprisingly, some of the brightest young minds on the planet are striving to join this remarkable enterprise in what promises to be among its greatest years. The Genetics Society of America should be at the forefront of all these developments. Genetic advances continue to unify all biological sciences, and a forum is needed to provide wise counsel, to nurture the careers of young geneticists, to communicate with the public, and to improve education, so more individuals can bring a true understanding of the biological world to today’s issues. There are several steps the GSA must take to provide this needed leadership. First, we must reach out and welcome every person who works to understand how genomes operate. We not only want a diverse membership, we need one. Splintering may succeed within ecosystems, but a tropical rainforest of genetics will not advance the future of our science, which is striving for unification. Most of the time we will continue to revel in our favorite realms, but we need a Genetics Society capable of overseeing the full scope of genetic science placing it all in its proper perspective.
    [Show full text]
  • Genome-Wide Rnai Screen Identifies Broadly-Acting Host Factors That Inhibit Arbovirus Infection." Plos Pathogens.10,2
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Digital Commons@Becker Washington University School of Medicine Digital Commons@Becker Open Access Publications 2014 Genome-wide RNAi screen identifies broadly- acting host factors that inhibit arbovirus infection Ari Yasunaga University of Pennsylvania Sheri L. Hanna University of Pennsylvania Jianqing Li Washington University School of Medicine in St. Louis Hyelim Cho Washington University School of Medicine in St. Louis Patrick P. Rose University of Pennsylvania See next page for additional authors Follow this and additional works at: http://digitalcommons.wustl.edu/open_access_pubs Recommended Citation Yasunaga, Ari; Hanna, Sheri L.; Li, Jianqing; Cho, Hyelim; Rose, Patrick P.; Spiridigliozzi, Anna; Gold, Beth; Diamond, Michael S.; and Cherry, Sara, ,"Genome-wide RNAi screen identifies broadly-acting host factors that inhibit arbovirus infection." PLoS Pathogens.10,2. e1003914. (2014). http://digitalcommons.wustl.edu/open_access_pubs/2700 This Open Access Publication is brought to you for free and open access by Digital Commons@Becker. It has been accepted for inclusion in Open Access Publications by an authorized administrator of Digital Commons@Becker. For more information, please contact [email protected]. Authors Ari Yasunaga, Sheri L. Hanna, Jianqing Li, Hyelim Cho, Patrick P. Rose, Anna Spiridigliozzi, Beth Gold, Michael S. Diamond, and Sara Cherry This open access publication is available at Digital Commons@Becker: http://digitalcommons.wustl.edu/open_access_pubs/2700 Genome-Wide RNAi Screen Identifies Broadly-Acting Host Factors That Inhibit Arbovirus Infection Ari Yasunaga1,2, Sheri L. Hanna1,2, Jianqing Li3, Hyelim Cho3, Patrick P. Rose1,2, Anna Spiridigliozzi1,2, Beth Gold1,2, Michael S.
    [Show full text]
  • 1 a Single Vertebrate DNA Virus Protein Disarms Invertebrate
    A single vertebrate DNA virus protein disarms invertebrate immunity to RNA virus infection Don B. Gammon1, Sophie Duraffour2, Daniel K. Rozelle3, Heidi Hehnly4, Rita Sharma1,9, Michael E. Sparks5, Cara C. West6, Ying Chen1, James J. Moresco7, Graciela Andrei2, John H. Connor3, Darryl Conte Jr1., Dawn E. Gundersen-Rindal5, William L. Marshall6,8#, John R. Yates III7, Neal Silverman6 and Craig C. Mello1,9,*. 1University of Massachusetts Medical School, RNA Therapeutics Institute, Worcester, MA, USA. 2Rega Institute for Medical Research, Leuven, Belgium. 3Boston University, Department of Microbiology, Boston, MA, USA. 4University of Massachusetts Medical School, Program in Molecular Medicine, Worcester, MA, USA. 5United States Department of Agriculture, Agricultural Research Service, Beltsville, MD, USA. 6University of Massachusetts Medical School, Department of Medicine, Worcester, MA, USA. 7The Scripps Research Institute, Department of Chemical Physiology, La Jolla, CA, USA. 8Merck Research Laboratories, Boston, MA, USA. #Current Address. 9Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA, USA. *Corresponding author: Please address all correspondence to Dr. Craig Mello at the University of Massachusetts Medical School. Email: [email protected]. Telephone: 508-856-1602. 1 1 Abstract 2 Virus-host interactions drive a remarkable diversity of immune responses and 3 countermeasures. We found that two RNA viruses with broad host ranges, vesicular 4 stomatitis virus (VSV) and Sindbis virus (SINV), are completely restricted in their 5 replication after entry into Lepidopteran cells. This restriction is overcome when cells 6 are co-infected with vaccinia virus (VACV), a vertebrate DNA virus. Using RNAi 7 screening, we show that Lepidopteran RNAi, Nuclear Factor-κB, and ubiquitin- 8 proteasome pathways restrict RNA virus infection.
    [Show full text]