The distribution of LAT in the human TG in this study contrasts with the mouse model, where A5+ neurons, which have a high co-localization with TrkA+ neurons, are more permissive for HSV-1 latent infection, whilst KH10+ neurons, which have a high co-localization with Ret+ neurons, are less permissive [18], [21], [23]. Here, IGKV2D-26 is linked to disease arising from reactivation of latent virus.