tetano
Editor, Senior Moderator
Cell Host Microbe
. 2022 Sep 6;S1931-3128(22)00419-X.
doi: 10.1016/j.chom.2022.09.002. Online ahead of print.
Antigenic characterization of the SARS-CoV-2 Omicron subvariant BA.2.75
Qian Wang[SUP] 1 [/SUP], Sho Iketani[SUP] 1 [/SUP], Zhiteng Li[SUP] 1 [/SUP], Yicheng Guo[SUP] 1 [/SUP], Andre Yanchen Yeh[SUP] 2 [/SUP], Michael Liu[SUP] 1 [/SUP], Jian Yu[SUP] 1 [/SUP], Zizhang Sheng[SUP] 1 [/SUP], Yaoxing Huang[SUP] 1 [/SUP], Lihong Liu[SUP] 3 [/SUP], David D Ho[SUP] 4 [/SUP]
Affiliations
Abstract
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron subvariant BA.2.75 emerged recently and appears to be spreading. It has nine mutations in spike compared with the currently circulating BA.2, raising concerns that it may further evade vaccine-elicited and therapeutic antibodies. We found BA.2.75 to be moderately more neutralization resistant to sera from vaccinated/boosted individuals than BA.2 (1.8-fold), similar to BA.2.12.1 (1.1-fold), but more neutralization sensitive than BA.4/5 (0.6-fold). Relative to BA.2, BA.2.75 showed heightened resistance to class 1 and class 3 monoclonal antibodies targeting the spike-receptor-binding domain while gaining sensitivity to class 2 antibodies. Resistance was largely conferred by G446S and R460K mutations. BA.2.75 was slightly resistant (3.7-fold) to bebtelovimab, a therapeutic antibody with potent activity against all Omicron subvariants. BA.2.75 also exhibited a higher binding affinity to host receptor ACE2 than other Omicron subvariants. BA.2.75 provides further insight into SARS-CoV-2 evolution as it gains transmissibility while incrementally evading antibody neutralization.
Keywords: ACE2 affinity; BA.2.75; COVID-19; Omicron; SARS-CoV-2; antibody evasion; monoclonal antibodies; serum neutralization; vaccine.
. 2022 Sep 6;S1931-3128(22)00419-X.
doi: 10.1016/j.chom.2022.09.002. Online ahead of print.
Antigenic characterization of the SARS-CoV-2 Omicron subvariant BA.2.75
Qian Wang[SUP] 1 [/SUP], Sho Iketani[SUP] 1 [/SUP], Zhiteng Li[SUP] 1 [/SUP], Yicheng Guo[SUP] 1 [/SUP], Andre Yanchen Yeh[SUP] 2 [/SUP], Michael Liu[SUP] 1 [/SUP], Jian Yu[SUP] 1 [/SUP], Zizhang Sheng[SUP] 1 [/SUP], Yaoxing Huang[SUP] 1 [/SUP], Lihong Liu[SUP] 3 [/SUP], David D Ho[SUP] 4 [/SUP]
Affiliations
- PMID: 36108630
- DOI: 10.1016/j.chom.2022.09.002
Abstract
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron subvariant BA.2.75 emerged recently and appears to be spreading. It has nine mutations in spike compared with the currently circulating BA.2, raising concerns that it may further evade vaccine-elicited and therapeutic antibodies. We found BA.2.75 to be moderately more neutralization resistant to sera from vaccinated/boosted individuals than BA.2 (1.8-fold), similar to BA.2.12.1 (1.1-fold), but more neutralization sensitive than BA.4/5 (0.6-fold). Relative to BA.2, BA.2.75 showed heightened resistance to class 1 and class 3 monoclonal antibodies targeting the spike-receptor-binding domain while gaining sensitivity to class 2 antibodies. Resistance was largely conferred by G446S and R460K mutations. BA.2.75 was slightly resistant (3.7-fold) to bebtelovimab, a therapeutic antibody with potent activity against all Omicron subvariants. BA.2.75 also exhibited a higher binding affinity to host receptor ACE2 than other Omicron subvariants. BA.2.75 provides further insight into SARS-CoV-2 evolution as it gains transmissibility while incrementally evading antibody neutralization.
Keywords: ACE2 affinity; BA.2.75; COVID-19; Omicron; SARS-CoV-2; antibody evasion; monoclonal antibodies; serum neutralization; vaccine.