Clinical Sequencing Uncovers Origins and Evolution of Lassa Virus.

Cell

Authors	Kristian Andersen B Jesse Shapiro Christian Matranga Rachel Sealfon Aaron Lin Lina Moses Onikepe Folarin Augustine Goba Ikponmwonsa Odia Philomena Ehiane Mambu Momoh Eleina England Sarah Winnicki Luis Branco Stephen Gire Eric Phelan Ridhi Tariyal Ryan Tewhey Omowunmi Omoniwa Mohammed Fullah Richard Fonnie Mbalu Fonnie Lansana Kanneh Simbirie Jalloh Michael Gbakie Sidiki Saffa Kandeh Karbo Adrianne Gladden James Qu Matthew Stremlau Mahan Nekoui Hilary Finucane Shervin Tabrizi Joseph Vitti Bruce Birren Michael Fitzgerald Caryn McCowan Andrea Ireland Aaron Berlin James Bochicchio Barbara Tazon-Vega Niall Lennon Elizabeth Ryan Zach Bjornson Danny Milner Amanda Lukens Nisha Broodie Megan Rowland Megan Heinrich Marjan Akdag John Schieffelin Danielle Levy Henry Akpan Daniel Bausch Kathleen Rubins Joseph McCormick Eric Lander Stephan Günther Lisa Hensley Sylvanus Okogbenin Viral Hemorrhagic Fever Consortium Stephen Schaffner Peter Okokhere S Humarr Khan Donald Grant George Akpede Danny Asogun Andreas Gnirke Joshua Levin Christian Happi Robert Garry Pardis Sabeti
Keywords	Animals Humans Mutation Genetic Variation Biological Evolution Ebolavirus Hemorrhagic Fever, Ebola Genome, Viral Viral Proteins Glycoproteins RNA, Viral Disease Reservoirs Lassa Fever Lassa virus Zoonoses Africa, Western Nigeria Murinae
Abstract	The 2013-2015 West African epidemic of Ebola virus disease (EVD) reminds us of how little is known about biosafety level 4 viruses. Like Ebola virus, Lassa virus (LASV) can cause hemorrhagic fever with high case fatality rates. We generated a genomic catalog of almost 200 LASV sequences from clinical and rodent reservoir samples. We show that whereas the 2013-2015 EVD epidemic is fueled by human-to-human transmissions, LASV infections mainly result from reservoir-to-human infections. We elucidated the spread of LASV across West Africa and show that this migration was accompanied by changes in LASV genome abundance, fatality rates, codon adaptation, and translational efficiency. By investigating intrahost evolution, we found that mutations accumulate in epitopes of viral surface proteins, suggesting selection for immune escape. This catalog will serve as a foundation for the development of vaccines and diagnostics. VIDEO ABSTRACT.
Year of Publication	2015
Journal	Cell
Volume	162
Issue	4
Pages	738-50
Date Published	2015 Aug 13
ISSN	1097-4172
URL	http://linkinghub.elsevier.com/retrieve/pii/S0092-8674(15)00897-1
DOI	10.1016/j.cell.2015.07.020
PubMed ID	26276630
PubMed Central ID	PMC4537774
Links	PubMed Google Scholar DOI
Grant list	R01 AI114855 / AI / NIAID NIH HHS / United States HHSN272201000022C / PHS HHS / United States HHSN272200900018C / AI / NIAID NIH HHS / United States 1DP2OD006514-01 / OD / NIH HHS / United States U19 AI109762 / AI / NIAID NIH HHS / United States K99 HG008179 / HG / NHGRI NIH HHS / United States HHSN272200900018C / PHS HHS / United States HHSN272201000022C / AI / NIAID NIH HHS / United States U19AI110818 / AI / NIAID NIH HHS / United States HHSN272200900049C / AI / NIAID NIH HHS / United States DP2 OD006514 / OD / NIH HHS / United States U19 AI110818 / AI / NIAID NIH HHS / United States HHSN272200900049C / PHS HHS / United States