Researchers used a SARS-CoV-2 spike protein-pseudotyped viral model to characterize BA.2.86 variant neutralization by monoclonal antibodies.
By Pooja Toshniwal PahariaSep 6 2023Reviewed by Sophia Coveney In a recent study posted to the bioRxiv* preprint server, researchers used a severe acute respiratory syndrome coronavirus 2 spike protein-pseudotyped viral model to characterize SARS-CoV-2 BA.2.86 variant neutralization by monoclonal antibodies and by sera obtained from Stockholm, inclusive of a recent group, and another group sampled before the XBB variant emerged in Sweden.
The development of the BA.2.86 variant is similar to the emergence of the SARS-CoV-2 Omicron BA.13 variant, with more than 30 amino acid substitutions within the spike glycoprotein in relation to the BA.2 variant, including many mutations in the main antigenic regions. For the study, a SARS-CoV-2 BA.2.86 variant spike glycoprotein-pseudotyped viral model was employed. The researchers assessed BA.2.86 neutralization by serum obtained from blood donor individuals in Stockholm at week 34 to describe the relative susceptibility of the BA.2.86 variant to antibody-mediated immune responses at a population level.
BA.2.86 mutations were discovered in comparison to BA.2. Sanger sequencing was used to validate and examine the nucleotide sequences for codon-optimized BA.2.86 spike protein constructions. Multiple site-directed mutagenesis was used to create the XBB.1.5 spike-encoding plasmid. For the culture studies, human embryonic kidney 293T cells expressing angiotensin-converting enzyme 2 were used.
Across all three types, ‘pre-XBB’ sampled sera had significantly lower neutralizing Ab titers compared to the recently obtained sera, with nine of the 12 samples from pre-XBB variant times having half-maximal inhibitory concentration titers below the detection cut-off.
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