TY - JOUR
T1 - Evolutionary analysis of the Delta and Delta Plus variants of the SARS-CoV-2 viruses
AU - Kannan, Saathvik R.
AU - Spratt, Austin N.
AU - Cohen, Alisha R.
AU - Naqvi, S. Hasan
AU - Chand, Hitendra S.
AU - Quinn, Thomas P.
AU - Lorson, Christian L.
AU - Byrareddy, Siddappa N.
AU - Singh, Kamal
N1 - Funding Information:
KS acknowledges support from the Office of Research, University of Missouri(Bond Life Sciences Center, Early Concept Grant). SNB acknowledges the independent research and development (IRAD) funding from the National Strategic Research Institute (NSRI) at the University of Nebraska. KS and TPQ acknowledge the computation facilities of the Molecular Interactions Core at the University of Missouri, Columbia, MO 65212. We thank the laboratories that have generously deposited sequences into the GISAID database. We thank Kamran S. Farid for the analysis of the antibody interaction with Spike protein.
Funding Information:
KS acknowledges support from the Office of Research, University of Missouri (Bond Life Sciences Center, Early Concept Grant). SNB acknowledges the independent research and development ( IRAD ) funding from the National Strategic Research Institute ( NSRI ) at the University of Nebraska. KS and TPQ acknowledge the computation facilities of the Molecular Interactions Core at the University of Missouri, Columbia, MO 65212. We thank the laboratories that have generously deposited sequences into the GISAID database. We thank Kamran S. Farid for the analysis of the antibody interaction with Spike protein.
Publisher Copyright:
© 2021 Elsevier Ltd
PY - 2021/11
Y1 - 2021/11
N2 - Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has been rapidly evolving in the form of new variants. At least eleven known variants have been reported. The objective of this study was to delineate the differences in the mutational profile of Delta and Delta Plus variants. High-quality sequences (n = 1756) of Delta (B.1.617.2) and Delta Plus (AY.1 or B.1.617.2.1) variants were used to determine the prevalence of mutations (≥20 %) in the entire SARS-CoV-2 genome, their co-existence, and change in prevalence over a period of time. Structural analysis was conducted to get insights into the impact of mutations on antibody binding. A Sankey diagram was generated using phylogenetic analysis coupled with sequence-acquisition dates to infer the migration of the Delta Plus variant and its presence in the United States. The Delta Plus variant had a significant number of high-prevalence mutations (≥20 %) than in the Delta variant. Signature mutations in Spike (G142D, A222V, and T95I) existed at a more significant percentage in the Delta Plus variant than the Delta variant. Three mutations in Spike (K417N, V70F, and W258L) were exclusively present in the Delta Plus variant. A new mutation was identified in ORF1a (A1146T), which was only present in the Delta Plus variant with ~58 % prevalence. Furthermore, five key mutations (T95I, A222V, G142D, R158G, and K417N) were significantly more prevalent in the Delta Plus than in the Delta variant. Structural analyses revealed that mutations alter the sidechain conformation to weaken the interactions with antibodies. Delta Plus, which first emerged in India, reached the United States through England and Japan, followed by its spread to more than 20 the United States. Based on the results presented here, it is clear that the Delta and Delta Plus variants have unique mutation profiles, and the Delta Plus variant is not just a simple addition of K417N to the Delta variant. Highly correlated mutations may have emerged to keep the structural integrity of the virus.
AB - Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has been rapidly evolving in the form of new variants. At least eleven known variants have been reported. The objective of this study was to delineate the differences in the mutational profile of Delta and Delta Plus variants. High-quality sequences (n = 1756) of Delta (B.1.617.2) and Delta Plus (AY.1 or B.1.617.2.1) variants were used to determine the prevalence of mutations (≥20 %) in the entire SARS-CoV-2 genome, their co-existence, and change in prevalence over a period of time. Structural analysis was conducted to get insights into the impact of mutations on antibody binding. A Sankey diagram was generated using phylogenetic analysis coupled with sequence-acquisition dates to infer the migration of the Delta Plus variant and its presence in the United States. The Delta Plus variant had a significant number of high-prevalence mutations (≥20 %) than in the Delta variant. Signature mutations in Spike (G142D, A222V, and T95I) existed at a more significant percentage in the Delta Plus variant than the Delta variant. Three mutations in Spike (K417N, V70F, and W258L) were exclusively present in the Delta Plus variant. A new mutation was identified in ORF1a (A1146T), which was only present in the Delta Plus variant with ~58 % prevalence. Furthermore, five key mutations (T95I, A222V, G142D, R158G, and K417N) were significantly more prevalent in the Delta Plus than in the Delta variant. Structural analyses revealed that mutations alter the sidechain conformation to weaken the interactions with antibodies. Delta Plus, which first emerged in India, reached the United States through England and Japan, followed by its spread to more than 20 the United States. Based on the results presented here, it is clear that the Delta and Delta Plus variants have unique mutation profiles, and the Delta Plus variant is not just a simple addition of K417N to the Delta variant. Highly correlated mutations may have emerged to keep the structural integrity of the virus.
KW - AY.1
KW - B.1.617.2
KW - B.1.617.2.1
KW - Delta plus variant
KW - Delta variant
KW - SARS-CoV-2
KW - Spike
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U2 - 10.1016/j.jaut.2021.102715
DO - 10.1016/j.jaut.2021.102715
M3 - Article
C2 - 34399188
AN - SCOPUS:85112303517
VL - 124
JO - Journal of Autoimmunity
JF - Journal of Autoimmunity
SN - 0896-8411
M1 - 102715
ER -