Author:
Liu Rong,Wu Pei,Ogrodzki Pauline,Mahmoud Sally,Liang Ke,Liu Pengjuan,Francis Stephen S.,Khalak Hanif,Liu Denghui,Li Junhua,Ma Tao,Chen Fang,Liu Weibin,Huang Xinyu,He Wenjun,Yuan Zhaorong,Qiao Nan,Meng Xin,Alqarni Budoor,Quilez Javier,Kusuma Vinay,Lin Long,Jin Xin,Yang Chongguang,Anton Xavier,Koshy Ashish,Yang Huanming,Xu Xun,Wang Jian,Xiao Peng,Al Kaabi Nawal,Fasihuddin Mohammed Saifuddin,Selvaraj Francis Amirtharaj,Weber Stefan,Al Hosani Farida Ismail,Liu Siyang,Zaher Walid Abbas
Abstract
AbstractTo unravel the source of SARS-CoV-2 introduction and the pattern of its spreading and evolution in the United Arab Emirates, we conducted meta-transcriptome sequencing of 1067 nasopharyngeal swab samples collected between May 9th and Jun 29th, 2020 during the first peak of the local COVID-19 epidemic. We identified global clade distribution and eleven novel genetic variants that were almost absent in the rest of the world and that defined five subclades specific to the UAE viral population. Cross-settlement human-to-human transmission was related to the local business activity. Perhaps surprisingly, at least 5% of the population were co-infected by SARS-CoV-2 of multiple clades within the same host. We also discovered an enrichment of cytosine-to-uracil mutation among the viral population collected from the nasopharynx, that is different from the adenosine-to-inosine change previously reported in the bronchoalveolar lavage fluid samples and a previously unidentified upregulation of APOBEC4 expression in nasopharynx among infected patients, indicating the innate immune host response mediated by ADAR and APOBEC gene families could be tissue-specific. The genomic epidemiological and molecular biological knowledge reported here provides new insights for the SARS-CoV-2 evolution and transmission and points out future direction on host–pathogen interaction investigation.
Publisher
Springer Science and Business Media LLC