Clinical Sequencing Uncovers Origins and Evolution of Lassa virus.
Cell. 2015 Aug 13;162(4):738-50. doi: 10.1016/j.cell.2015.07.020.
Andersen KG, Shapiro BJ, Matranga CB, Sealfon R, Lin AE, Moses LM, Folarin OA, Goba A, Odia I, Ehiane PE, Momoh M, England EM, Winnicki S, Branco LM, Gire SK, Phelan E, Tariyal R, Tewhey R, Omoniwa O, Fullah M, Fonnie R, Fonnie M, Kanneh L, Jalloh S, Gbakie M, Saffa S, Karbo K, Gladden AD, Qu J, Stremlau M, Nekoui M, Finucane HK, Tabrizi S, Vitti JJ, Birren B, Fitzgerald M, McCowan C, Ireland A, Berlin AM, Bochicchio J, Tazon-Vega B, Lennon NJ, Ryan EM, Bjornson Z, Milner DA Jr, Lukens AK, Broodie N, Rowland M, Heinrich M, Akdag M, Schieffelin JS, Levy D, Akpan H, Bausch DG, Rubins K, McCormick JB, Lander ES, Günther S, Hensley L, Okogbenin S; Viral Hemorrhagic Fever Consortium, Schaffner SF, Okokhere PO, Khan SH, Grant DS, Akpede GO, Asogun DA, Gnirke A, Levin JZ, Happi CT, Garry RF, Sabeti PC.
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.