Ebola Virus Replication and Disease Without Immunopathology in Mice Expressing Transgenes to Support Human Myeloid and Lymphoid Cell Engraftment.
Document Type
Article
Publication Date
10-15-2016
JAX Location
Reprint Collection
JAX Source
J Infect Dis 2016 Oct 15; 214(suppl3):S308-S318.
Volume
214
Issue
suppl 3
First Page
308
Last Page
308
ISSN
0022-1899
PMID
27601621
Abstract
The study of Ebola virus (EBOV) pathogenesis in vivo has been limited to nonhuman primate models or use of an adapted virus to cause disease in rodent models. Herein we describe wild-type EBOV (Makona variant) infection of mice engrafted with human hematopoietic CD34(+) stem cells (Hu-NSG™-SGM3 mice; hereafter referred to as SGM3 HuMice). SGM3 HuMice support increased development of myeloid immune cells, which are primary EBOV targets. In SGM3 HuMice, EBOV replicated to high levels, and disease was observed following either intraperitoneal or intramuscular inoculation. Despite the high levels of viral antigen and inflammatory cell infiltration in the liver, the characteristic histopathology of Ebola virus disease was not observed, and this absence of severe immunopathology may have contributed to the recovery and survival of some of the animals. Future investigations into the underlying mechanisms of the atypical disease presentation in SGM3 HuMice will provide additional insights into the immunopathogenesis of severe EBOV disease. J Infect Dis 2016 Oct 15; 214(suppl3):S308-S318.
Recommended Citation
Spengler J,
Lavender K,
Martellaro C,
Carmody A,
Kurth A,
Keck JG,
Saturday G,
Scott D,
Nichol S,
Hasenkrug K,
Spiropoulou C,
Feldmann H,
Prescott J.
Ebola Virus Replication and Disease Without Immunopathology in Mice Expressing Transgenes to Support Human Myeloid and Lymphoid Cell Engraftment. J Infect Dis 2016 Oct 15; 214(suppl3):S308-S318.