Coding-Complete Genome Sequences of a Delta Subvariant (AY.33) of SARS-CoV-2 Obtained from Moroccan COVID-19 Patients

ABSTRACT We report here the complete genome sequences of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) strains obtained from Moroccan patients with COVID-19. The analysis of these sequences indicates that the identified strains belong to the AY.33 sublineage of the Delta variant.

content of 37.9%. The quality of the sequences was monitored using the Nextclade web tool version 1.7.2 (https://clades.nextstrain.org), although the determination of the mutations was carried out using the web application Cov-GLUE (http://cov-glue.cvr.gla.ac.uk/), and the lineage and sublineage were obtained using the web application Pangolin (https://pangolin.cog-uk.io/).
The genomes of both samples accumulated 4 new amino acid changes within the Spike protein (T29A, T50I, T299I, and Q613) in addition to the 10 modifications that characterize the Delta 2 variant. T487K, which results in a significant modification in the conformation of the receptor binding domain (RBD), was linked to an increase in RBD binding affinity to the cell surface  S  T19R  T29A  G142D  R158G  T250I  T299I  L452R  T478K  Q613H  D614G  P681R  D950N  E157-F158-T19R  T29A  G142D  R158G  T250I  T299I  L452R  T478K  Q613H  D614G  P681R  D950N  E156-F157-ORF 3a  S26L  S26L   M  I82T   ORF 7a  V82A  T120I   V82A  T120I   ORF 7b  T40I  T40I   ORF 8  D119-F120-ORF 9B  T60A  T60A   N  D63G  R203M  G215C  N377Y   D63G  R203M  G215C  N377Y angiotensin converting enzyme 2 (ACE2) receptor (3). In addition, Q613H was also reported as an amino acid modification of little-known impact; however, given its close proximity to the well-known D614G, it is possible that this amino acid change would enhance the role of the latter in terms of virus transmissibility (4,5). Furthermore, among amino acid modifications affecting the receptor binding motif (RBM) region, L452R is present in variants which exhibit high binding affinity to the ACE2 receptor and may also contribute to humoral immune escape (6). Another interesting amino acid change is P681R, located between subunits S1 and S2. It has been established that the P681R change increases S1/S2 cleavage, which induces a quicker fusion between virus and cell membrane, thus facilitating viral transmissibility (7).
Finally, the N-terminal domain (NTD) (an essential binding site for antibody 4A8 [8]) is altered through G142D. This mutation contributes to changing the structure of the NTD, resulting in the binding prevention of neutralization antibodies (NAb) to this domain (9). The characteristic B.1.617.2 and B.1.617.3 deletions 157 to 158 can also be observed and constitute another mechanism by which the virus acquired vaccine escape abilities (10).
The emergence and spread of new variants derived from volatile organic compounds (VOCs) are a global concern, their escape from vaccination is not yet well studied, and the genomic surveillance of the genome of SARS-CoV-2 remains a primary approach to identify variants and prevent their spread.
Data availability. The SARS-CoV-2 genome sequences 5858 and 5900 were deposited into the GISAID database under the identifiers EPI_ISL_6002899 and EPI_ISL_6002900, respectively, and in NCBI GenBank under the accession numbers OL375239 and OL375240, respectively. Raw reads from next-generation sequencing (NGS) are available in the BioProject database under SRA number PRJNA780922. The specific raw read library identifiers of samples 5858 and 5900 are SRX13150847 and SRX13150848, respectively.

ACKNOWLEDGMENT
This study was supported and financed by the Hassan II Academy of Science and Technology, Morocco.