Project description:The unprecedented magnitude of the 2013-2016 Makona Ebola virus (M-EBOV) epidemic likely resulted from multiple epidemiologic factors that set it apart from previous outbreaks. Nonetheless, genetic adaptations that distinguish M-EBOV from previous isolates may also have contributed to the scale of the epidemic. Of particular interest is a M-EBOV glycoprotein (GP) variant, GP-A82V, that was first detected at the inflection point of the 2013-2016 outbreak - when the number of cases increased exponentially - and which completely supplanted the earlier M-EBOV sequence. We found that, as compared with the earlier strain, GP-A82V increased the ability of M-EBOV to fuse with and infect cells of primate origin, including human blood dendritic cells, without altering innate immune signaling in target cells. Residue 82 is located at the NPC1-binding site on M-EBOV GP and the increased infectivity of GP-A82V was restricted to cells from species in which the NPC1 orthologue bears primate-defining residues at the critical interface. We utilized HIV-derived lentiviral vectors pseudotyped with founder and A82V containing M-EBOV GPs to explore the potential that this modification alters how human monocyte-derived dendritic cells (MDDCs) respond to EBOV GP stimulation.

2017-08-31 | GSE84865 | GEO

Negative Mood Is Associated with Diet and Dietary Antioxidants in University Students During the Menstrual Cycle: A Cross-Sectional Study from Guangzhou, China.

Project description: Not available

| S-EPMC7023165 | biostudies-literature

Human Adaptation of Ebola Virus during the West African Outbreak.

Project description: Not available

| S-EPMC5101188 | biostudies-literature

Perspectives on West Africa Ebola Virus Disease Outbreak, 2013-2016.

Project description: Not available

| S-EPMC4880067 | biostudies-literature

Clinical and epidemiological features of the 2014 large-scale dengue outbreak in Guangzhou city, China.

Project description: Not available