Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, Rocky Mountain Laboratories, Hamilton, MT, USA.
Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, Rocky Mountain Laboratories, Hamilton, MT, USA.
Cell Rep. 2018 May 8;23(6):1806-1816. doi: 10.1016/j.celrep.2018.04.027.
Ebola virus (EBOV), isolate Makona, the causative agent of the West African EBOV epidemic, has been the subject of numerous investigations to determine the genetic diversity and its potential implication for virus biology, pathogenicity, and transmissibility. Despite various mutations that have emerged over time through multiple human-to-human transmission chains, their biological relevance remains questionable. Recently, mutations in the glycoprotein GP and polymerase L, which emerged and stabilized early during the outbreak, have been associated with improved viral fitness in cell culture. Here, we infected mice and rhesus macaques with EBOV-Makona isolates carrying or lacking those mutations. Surprisingly, all isolates behaved very similarly independent of the genotype, causing severe or lethal disease in mice and macaques, respectively. Likewise, we could not detect any evidence for differences in virus shedding. Thus, no specific biological phenotype could be associated with these EBOV-Makona mutations in two animal models.
埃博拉病毒（EBOV），马科纳株，是西非埃博拉病毒疫情的病原体，已经成为众多研究的主题，以确定其遗传多样性及其对病毒生物学、致病性和传染性的潜在影响。尽管随着时间的推移，通过多次人与人之间的传播链出现了各种突变，但它们的生物学相关性仍存在疑问。最近，在疫情早期出现并稳定下来的糖蛋白 GP 和聚合酶 L 中的突变与病毒在细胞培养中的适应性提高有关。在这里，我们用携带或不携带这些突变的 EBOV-Makona 分离株感染小鼠和恒河猴。令人惊讶的是，所有分离株的行为非常相似，与基因型无关，分别导致小鼠和恒河猴发生严重或致命疾病。同样，我们也没有发现病毒脱落存在差异的任何证据。因此，在两个动物模型中，这些 EBOV-Makona 突变并没有与任何特定的生物学表型相关联。
