Genomic epidemiology of SARS-CoV-2 in the UAE reveals novel virus mutation, patterns of co-infection and tissue specific host immune response

Rong Liu,Wenjun He,Jian Wang,Farida Ismail Al Hosani,Pengjuan Liu,Nan Qiao,Weibin Liu,Ashish Koshy,Xavier Anton,Pauline Ogrodzki,Hanif Khalak,Vinay Kusuma,Denghui Liu,Junhua Li,Xin Jin,Francis Amirtharaj Selvaraj,Li Lin ,Xin Meng,Mohammed Saifuddin Fasihuddin,Chongguang Yang,Stefan Weber,Tao Ma,Siyang Liu,Budoor Alqarni,Javier Quilez,Huanming Yang,Xun Xu,Fang Chen,Stephen Francis ,Nawal Al Kaabi,Zhaorong Yuan,Peng Xiao,Pei‐Ju Wu ,Ke Liang,S A Mahmoud ,Xinyu Huang,Walid Zaher

doi:10.1038/s41598-021-92851-3

Abstract

To 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.

Highlights

To 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
A total of 1067 nasopharyngeal swab samples collected from SARS-CoV-2 positive patients between May 7th and June 29th 2020 in Abu Dhabi were sequenced (Fig. 1A)
Quality of the genome assemblies was closely related to the sample viral load as measured by reads per million (RPM) and qRT-PCR Ct values (Fig. 1B, Fig. S2)

Summary

Introduction

To 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. To understand the transmission and infection dynamics of SARS-CoV-2 within the UAE and in relation to other countries, during April and July, 2020, we randomly collected 1067 nasopharyngeal specimens from SARSCoV-2 positive patients from the RT-qPCR screening program and conducted meta-transcriptomic sequencing. Our main scientific questions include (1) What is the virus genetic diversity and transmission pattern in the UAE during the first peak of the epidemic (2) What is the extent of co-infection of multiple SARS-CoV-2 variants in this international travel hub (3) Is there any innate immune host response to the SARS-CoV-2 infection that can be detected using the meta-transcriptomic sequencing, which contains both the host and the viral gene expression information

Methods

Results

Conclusion