January 10, 2013
Scientists engineer the Schmallenberg virus genome to understand how to reduce disease caused by the virus.
Researchers from the MRC Centre for Virus Research at the University of Glasgow in Scotland have developed methods to synthesize and change the genome of Schmallenberg virus (SBV). SBV is a recently discovered pathogen of livestock such as cattle, sheep and goats. The researchers have laid bare important ways by which this virus causes disease. The full report about the study publishes on January 10 in the Open Access journal, PLOS Pathogens.
SBV is of great concern because it causes stillbirths, abortions and fetal defects in pregnant cows and ewes. It has spread rapidly throughout Europe since its discovery in Germany less than eighteen months ago (in October 2011).
The new study describes researchers' use of molecular biological methods to design and assemble the viral "genome" completely in a test tube in a form that can be easily introduced and replicated in cultured cells. From these cells the researchers recovered virus with identical infection properties to the "natural" SBV. This approach, known as 'reverse genetics', allowed them to control the viral genome and identify a gene (called NSs) involved in protecting the virus against the immune response of infected animals. The researchers made viruses missing the NSs gene and found they made mice in the laboratory less sick than viruses containing the NSs gene. The researchers also discovered that SBV rapidly grows in the brain and spinal cord of aborted lambs and calves. The virus prefers to infect cells called neurons, which explains why it infects and damages the brain. This also results in muscular defects such as abnormally flexed legs often seen in stillborn animals when virus is transmitted from an SBV infected mother to the calves or lambs in the uterus during pregnancy.
Scottish researchers, led by Massimo Palmarini and Alain Kohl, suggest that the ability to engineer and control the SBV genome will allow the future development of new vaccines for this virus that is of great concern to European farmers. This work was conducted in collaboration with scientists in Italy at the Istituto G. Caporale and Germany (University of Veterinary Medicine in Hannover and the Friedrich Loeffler Institut).
FINANCIAL DISCLOSURE: This work was funded by the MRC and Wellcome Trust. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
COMPETING INTERESTS: The authors have declared that no competing interests exist.
PLEASE ADD THIS LINK TO THE PUBLISHED ARTICLE IN ONLINE VERSIONS OF YOUR REPORT: http://dx.plos.org/10.1371/journal.ppat.1003133 (link will go live upon embargo lift)
CITATION: Varela M, Schnettler E, Caporale M, Murgia C, Barry G, et al. (2013) Schmallenberg Virus Pathogenesis, Tropism and Interaction with the Innate Immune System of the Host. PLoS Pathog 9(1): e1003133. doi:10.1371/journal.ppat.1003133
Author contact:
Massimo Palmarini, University of Glasgow
+44 (0)141-330 2541 (or 4645)
massimo.palmarini@glasgow.ac.uk
PLOS Pathogens Contact:
Gina Alvino
(415) 568-3173
plospathogens@plos.org
Disclaimer
This press release refers to an upcoming article in PLOS Pathogens. The release is provided by the article authors. Any opinions expressed in these releases or articles are the personal views of the journal staff and/or article contributors, and do not necessarily represent the views or policies of PLOS. PLOS expressly disclaims any and all warranties and liability in connection with the information found in the releases and articles and your use of such information.
Media Permissions
PLOS Journals publish under a Creative Commons Attribution License, which permits free reuse of all materials published with the article, so long as the work is cited (e.g., Kaltenbach LS et al. (2007) Huntingtin Interacting Proteins Are Genetic Modifiers of Neurodegeneration. PLoS Genet 3(5): e82. doi:10.1371/journal.pgen.0030082). No prior permission is required from the authors or publisher. For queries about the license, please contact the relative journal contact indicated here: http://www.plos.org/about/media-inquiries/.
About PLOS Pathogens
PLOS Pathogens publishes outstanding original articles that significantly advance the understanding of pathogens and how they interact with their host organisms. All works published in PLOS Pathogens are open access. Everything is immediately available subject only to the condition that the original authorship and source are properly attributed. Copyright is retained by the authors. The Public Library of Science uses the Creative Commons Attribution License.
About the Public Library of Science
The Public Library of Science (PLOS) is a non-profit organization of scientists and physicians committed to making the world's scientific and medical literature a freely available public resource. For more information, visit http://www.plos.org
PLEASE MENTION THE OPEN-ACCESS JOURNAL PLOS Pathogens AS THE SOURCE FOR THIS ARTICLE AND PROVIDE A LINK TO THE FREELY AVAILABLE TEXT. THANK YOU.
Journal
PLoS Pathogens