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To the Editor: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) subvariant BA.2.86 was first reported in Denmark early in August 2023.1 By August 30, a total of 24 cases had been detected in 8 countries. BA.2.86 has a heavily mutated spike protein, with 29 substitutions, 4 deletions, and 1 insertion as compared with its putative ancestor, BA.2, which suggests a strong capacity to evade vaccine- and infection-induced antibodies.2 By the end of August in Sweden, BA.2.86 infections had been reported in 4 patients in different parts of the country. None of the patients had recently traveled abroad, which indicated a geographical spread within Sweden. The first verified Swedish BA.2.86 infection was detected on August 7 through a screening program within the Covid-19 Immunity (COMMUNITY) cohort study, which involved 2149 health care workers in Sweden. In this screening substudy, 297 participants in the cohort were tested for SARS-CoV-2 infection if they had upper respiratory symptoms3-5 (see the Supplementary Appendix, available with the full text of this letter at NEJM.org). The first participant in whom BA.2.86 infection was identified (index case) was an immunocompetent woman without chronic disorders who reported having rhinorrhea, chills, and fever with a symptom duration of 3 days. These symptoms were milder than those she had during a SARS-CoV-2 infection the previous year. Her husband and son also became ill with similar symptoms at the same time but were not tested.

unocompetent woman without chronic disorders who reported having rhinorrhea, chills, and fever with a symptom duration of 3 days. These symptoms were milder than those she had during a SARS-CoV-2 infection the previous year. Her husband and son also became ill with similar symptoms at the same time but were not tested. In addition to the previous infection, the index case had received four doses of the BNT162b2 vaccine (Pfizer–BioNTech) before the diagnosis of the BA.2.86 infection. A detailed immune history that was available through the previous collection of study samples3-5 revealed that she had a history of having serum IgG and mucosal IgA levels similar to those in the full COMMUNITY cohort before the BA.2.86 infection (Figure 1A and Tables S1 and S2 in the Supplementary Appendix). We next investigated whether BA.2.86 infection could boost nucleocapsid and spike-specific antibody responses. Serum and mucosal samples that had been obtained 3 weeks after infection in the index case were analyzed for wild-type nucleocapsid IgG and wild-type and BA.5 spike IgA and IgG. We compared the levels with those obtained in February 2023 and noted an increase by a factor of 36 in nucleocapsid IgG titers in serum (Figure 1B) and a stronger induction of mucosal IgA binding to wild-type and BA.5 spike proteins (factor increase, 3.6 and 3.4, respectively) as compared with serum IgG binding to wild-type and BA.5 spike proteins (factor increase, 1.1 and 1.5, respectively) (Figure 1C).

factor of 36 in nucleocapsid IgG titers in serum (Figure 1B) and a stronger induction of mucosal IgA binding to wild-type and BA.5 spike proteins (factor increase, 3.6 and 3.4, respectively) as compared with serum IgG binding to wild-type and BA.5 spike proteins (factor increase, 1.1 and 1.5, respectively) (Figure 1C). These findings suggest that BA.2.86 infection can substantially boost antibody responses. The results also confirm that highly vaccinated and previously infected immunocompetent persons with normal antibody levels can be infected with BA.2.86, which reveals the potential for BA.2.86 to cause a global surge in cases. Close monitoring is warranted to evaluate the effectiveness of the forthcoming and updated vaccines with respect to the BA.2.86 subvariant.