Ebola Virus Glycoprotein with Increased Infectivity Dominated the 2013-2016 Epidemic

被引：140

作者：

Diehl, William E. ^{[1
]}

Lin, Aaron E. ^{[2
,3
]}

Grubaugh, Nathan D. ^{[4
]}

Carvalho, Luiz Max ^{[5
]}

Kim, Kyusik ^{[1
]}

Kyawe, Pyae Phyo ^{[6
]}

McCauley, Sean M. ^{[1
]}

Donnard, Elisa ^{[1
,7
]}

Kucukural, Alper ^{[1
,7
]}

McDonel, Patrick ^{[1
,7
]}

Schaffner, Stephen F. ^{[2
,3
]}

Garber, Manuel ^{[1
,7
]}

Rambaut, Andrew ^{[5
]}

Andersen, Kristian G. ^{[2
,4
,8
]}

Sabeti, Pardis C. ^{[2
,3
]}

Luban, Jeremy ^{[1
]}

机构：

[1] Univ Massachusetts, Sch Med, Program Mol Med, 373 Plantat St, Worcester, MA 01605 USA

[2] Broad Inst Harvard & MIT, 75 Ames St, Cambridge, MA 02142 USA

[3] Harvard Univ, 52 Oxford St, Cambridge, MA 02138 USA

[4] Scripps Res Inst, Dept Immunol & Microbial Sci, 10550 North Torrey Pines Rd, La Jolla, CA 92037 USA

[5] Univ Edinburgh, Inst Evolutionary Biol, Ashworth Labs, Kings Bldg,West Mains Rd, Edinburgh EH9 3JT, Midlothian, Scotland

[6] Univ Massachusetts, Sch Med, Dept Med, 55 Lake Ave North, Worcester, MA 01605 USA

[7] Univ Massachusetts, Sch Med, Program Bioinformat & Integrat Biol, Worcester, MA 01655 USA

[8] Scripps Translat Sci Inst, 3344 North Torrey Pines Court, La Jolla, CA 92037 USA

来源：

CELL | 2016年 / 167卷 / 04期

基金：

美国国家科学基金会;

关键词：

NIEMANN-PICK C1; HEMORRHAGIC-FEVER; INFLUENZA-VIRUS; CYNOMOLGUS MACAQUES; LENTIVIRAL VECTORS; RECEPTOR-BINDING; DENDRITIC CELLS; FRUIT BATS; VIRAL LOAD; TRANSMISSION;

D O I：

10.1016/j.cell.2016.10.014

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The magnitude of the 2013-2016 Ebola virus disease (EVD) epidemic enabled an unprecedented number of viral mutations to occur over successive human-to- human transmission events, increasing the probability that adaptation to the human host occurred during the outbreak. We investigated one nonsynonymous mutation, Ebola virus (EBOV) glycoprotein (GP) mutant A82V, for its effect on viral infectivity. This mutation, located at the NPC1-binding site on EBOV GP, occurred early in the 2013-2016 outbreak and rose to high frequency. We found that GP-A82V had heightened ability to infect primate cells, including human dendritic cells. The increased infectivity was restricted to cells that have primate-specific NPC1 sequences at the EBOV interface, suggesting that this mutation was indeed an adaptation to the human host. GP-A82V was associated with increased mortality, consistent with the hypothesis that the heightened intrinsic infectivity of GP-A82V contributed to disease severity during the EVD epidemic.

引用

页码：1088 / +

页数：17

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