Middle East respiratory syndrome coronavirus (MERS-CoV) causes a zoonotic respiratory disease of global public health concern, and dromedary camels are the only proven source of zoonotic infection. Although MERS-CoV infection is ubiquitous in dromedaries across Africa as well as in the Arabian Peninsula, zoonotic disease appears confined to the Arabian Peninsula. MERS-CoVs from Africa have hitherto been poorly studied. We genetically and phenotypically characterized MERS-CoV from dromedaries sampled in Morocco, Burkina Faso, Nigeria, and Ethiopia. Viruses from Africa (clade C) are phylogenetically distinct from contemporary viruses from the Arabian Peninsula (clades A and B) but remain antigenically similar in microneutralization tests. Viruses from West (Nigeria, Burkina Faso) and North (Morocco) Africa form a subclade, C1, that shares clade-defining genetic signatures including deletions in the accessory gene ORF4b. Compared with human and camel MERS-CoV from Saudi Arabia, virus isolates from Burkina Faso (BF785) and Nigeria (Nig1657) had lower virus replication competence in Calu-3 cells and in ex vivo cultures of human bronchus and lung. BF785 replicated to lower titer in lungs of human DPP4-transduced mice. A reverse genetics-derived recombinant MERS-CoV (EMC) lacking ORF4b elicited higher type I and III IFN responses than the isogenic EMC virus in Calu-3 cells. However, ORF4b deletions may not be the major determinant of the reduced replication competence of BF785 and Nig1657. Genetic and phenotypic differences in West African viruses may be relevant to zoonotic potential. There is an urgent need for studies of MERS-CoV at the animal–human interface.

中东呼吸综合征冠状病毒 (MERS-CoV) 引起全球公共卫生关注的人畜共患呼吸道疾病，单峰骆驼是唯一经证实的人畜共患感染源。尽管 MERS-CoV 感染在非洲和阿拉伯半岛的单峰骆驼中无处不在，但人畜共患疾病似乎仅限于阿拉伯半岛。迄今为止，对来自非洲的 MERS-CoV 的研究很少。我们从摩洛哥、布基纳法索、尼日利亚和埃塞俄比亚采样的单峰骆驼中对 MERS-CoV 进行了遗传和表型表征。来自非洲的病毒（进化枝 C）在系统发育上与来自阿拉伯半岛的当代病毒（进化枝 A 和 B）不同，但在微量中和试验中保持抗原性相似。来自西非（尼日利亚、布基纳法索）和北非（摩洛哥）的病毒形成一个分支，C1，ORF4b。与来自沙特阿拉伯的人类和骆驼 MERS-CoV 相比，来自布基纳法索 (BF785) 和尼日利亚 (Nig1657) 的病毒分离株在 Calu-3 细胞以及人类支气管和肺的离体培养物中具有较低的病毒复制能力。BF785 在人 DPP4 转导小鼠的肺中复制以降低滴度。与 Calu-3 细胞中的同基因 EMC 病毒相比，缺乏ORF4b的反向遗传学衍生的重组 MERS-CoV (EMC)引发了更高的 I 型和 III 型干扰素反应。然而，ORF4b缺失可能不是 BF785 和 Nig1657 复制能力降低的主要决定因素。西非病毒的遗传和表型差异可能与人畜共患病的可能性有关。迫切需要在动物 - 人机界面上研究 MERS-CoV。