Lubinski Bailey, Frazier Laura E, Phan My V T, Bugembe Daniel L, Cunningham Jessie L, Tang Tiffany, Daniel Susan, Cotten Matthew, Jaimes Javier A, Whittaker Gary R
Graduate Program in Biological & Biomedical Sciences, Cornell University, Ithaca, NY, 14853, USA.
Department of Microbiology & Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA.
bioRxiv. 2022 Mar 28:2021.06.30.450632. doi: 10.1101/2021.06.30.450632.
The African continent like all other parts of the world with high infection/low vaccination rates can, and will, be a source of novel SARS-CoV-2 variants. The A.23 viral lineage, characterized by three spike mutations F157L, V367F and Q613H, was first identified in COVID-19 cases from a Ugandan prison in July 2020, and then was identified in the general population with additional spike mutations (R102I, L141F, E484K and P681R) to comprise lineage A.23.1 by September 2020, with this virus being designated a variant of interest (VOI) in Africa and with subsequent spread to 26 other countries. The P681R spike substitution of the A.23.1 VOI is of note as it increases the number of basic residues in the sub-optimal SARS-CoV-2 spike protein furin cleavage site; as such, this substitution may affect viral replication, transmissibility or pathogenic properties. The same P681R substitution has also appeared in B.1.617 variants, including B.1.617.2 (Delta). Here, we performed assays using fluorogenic peptides mimicking the S1/S2 sequence from A.23.1 and B.1.617.2 and observed significantly increased cleavability with furin, compared to sequences derived from the original Wuhan-Hu1 S1/S2. We performed functional infectivity assays using pseudotyped MLV particles harboring SARS-CoV-2 spike proteins and observed an increase in transduction for A.23.1-pseudotyped particles compared to Wuhan-Hu-1 in Vero-TMPRSS2 and Calu-3 cells (with a presumed early entry pathway), although lowered infection in Vero E6 cells (with a presumed late entry pathway). However, these changes in infectivity were not reproduced in the original Wuhan-Hu-1 spike bearing only the P681R substitution. Our findings suggest that while A.23.1 has increased furin-mediated cleavage linked to the P681R substitution, which may affect viral infection and transmissibility, this substitution alone is not sufficient and needs to occur on the background of other spike protein changes to enable its full functional consequences.
与世界上所有感染率高/疫苗接种率低的地区一样,非洲大陆可能且将会成为新型严重急性呼吸综合征冠状病毒2(SARS-CoV-2)变体的来源。A.23病毒谱系以三个刺突突变F157L、V367F和Q613H为特征,于2020年7月在乌干达一所监狱的新冠肺炎病例中首次发现,然后在普通人群中发现了额外的刺突突变(R102I、L141F、E484K和P681R),到2020年9月形成了A.23.1谱系,这种病毒在非洲被指定为关注变体(VOI),随后传播到其他26个国家。A.23.1 VOI的P681R刺突替代值得注意,因为它增加了次优SARS-CoV-2刺突蛋白弗林蛋白酶切割位点中的碱性残基数量;因此,这种替代可能会影响病毒的复制、传播性或致病特性。相同的P681R替代也出现在B.1.617变体中,包括B.1.617.2(德尔塔)。在这里,我们使用模拟A.23.1和B.1.617.2的S1/S2序列的荧光肽进行了测定,与源自原始武汉-胡1 S1/S2的序列相比,观察到弗林蛋白酶的切割能力显著增加。我们使用携带SARS-CoV-2刺突蛋白的假型莫洛尼鼠白血病病毒(MLV)颗粒进行了功能感染性测定,在Vero-TMPRSS2和Calu-3细胞(推测为早期进入途径)中,观察到A.23.1假型颗粒的转导能力相对于武汉-胡1有所增加,尽管在Vero E6细胞(推测为晚期进入途径)中的感染有所降低。然而,仅携带P681R替代的原始武汉-胡1刺突并未重现这些感染性变化。我们的研究结果表明,虽然A.23.1与P681R替代相关的弗林蛋白酶介导的切割增加,这可能会影响病毒感染和传播性,但仅这种替代是不够的,需要在其他刺突蛋白变化的背景下发生才能产生其全部功能后果。