This article is based on a preprint posted to bioRxiv and has not been peer reviewed. Findings are preliminary and should not be used to guide clinical or public-health decisions.

A new SARS-CoV-2 sublineage called BA.3.2.2 — a heavily mutated Omicron descendant — is turning up disproportionately in children compared with adults, according to a preprint from Yunlong Cao’s immunology group at Peking University. Genomic surveillance reviewed in the paper shows BA.3.2.2 is significantly enriched in pediatric populations globally, unlike concurrent variants XFG and NB.1.8.1, which circulate more evenly across age groups.

The mechanism appears rooted in immune imprinting — the way a first SARS-CoV-2 encounter shapes all subsequent antibody responses. Adults who were infected with or vaccinated against the original Wuhan ancestral strain built up antibodies encoded by a germline gene segment called IGHV3-53/66. These broadly cross-reactive antibodies recognise a part of BA.3.2.2’s spike protein that the virus has not yet mutated away. Children born after 2021, however, were first exposed to Omicron subvariants — never to the ancestral strain — and their immune systems instead generated antibodies encoded by different gene segments (IGHV2-5 and IGHV5-51). Those Omicron-specific antibodies neutralise dominant current strains well, but BA.3.2.2 appears to have evolved in a way that evades them almost entirely, resulting in markedly lower neutralising titres against this specific variant in younger children.

A companion preprint from Columbia University (Wu et al.) used pseudovirus neutralisation assays across 36 participants spanning adults, school-age children (ages 3–10), and infants and toddlers (ages 6–28 months) and independently confirmed lower geometric mean titres against BA.3.2.2 specifically in both paediatric cohorts, while titres against NB.1.8.1 and XFG were comparable across all age groups.

The Cao lab paper raises a concern that if BA.3.2.2 sustains transmission in children, it could accumulate further mutations capable of also evading IGHV3-53/66 antibodies, potentially enabling wider cross-age transmission. The authors argue the findings may inform paediatric booster strategy. No specific booster recommendation is made; these are preliminary findings requiring peer review.

Primary source: Niu X. et al., “Lack of ancestral SARS-CoV-2 imprinting promotes BA.3.2.2 infection in children,” bioRxiv 2026. DOI: 10.64898/2026.06.05.730251. Not peer reviewed.