SARS-CoV-2 Omicron EG.5 and JN.1 induce enhanced pathogenicity in K18-hACE2 mice compared with the early Omicron subvariants

A new publication in Nature Lab Animal from C2i’s Alex Chin and Leo Poon demonstrates that the emerging SARS‑CoV‑2 Omicron EG.5 and JN.1 variants induce enhanced pathogenicity in K18‑hACE2 mice, overcoming limitations of early Omicron models and enabling more robust preclinical assessment of vaccines and antivirals.

Abstract:

The reduced pathogenicity of early SARS-CoV-2 Omicron subvariants in human ACE2-expressing K18-hACE2 mice has posed challenges for assessing vaccine and antiviral efficacy against the Omicron variant with the mouse model. Here we report the enhanced pathogenicity of the Omicron JN.1 and EG.5 lineages in K18-hACE2 mice compared with their ancestors, suggesting the potential of applying these Omicron lineages in the mouse infection model.

>>> SARS-CoV-2 Omicron EG.5 and JN.1 induce enhanced pathogenicity in K18-hACE2 mice compared with the early Omicron subvariants