(3-5), and, at the same time, in promoting neuronal survival after HSV-1 infection by reducing apoptosis (6). In vitro, the antiapoptotic effects of LAT are mediated by the inhibition of caspase-3, -8,-and -9-induced apoptosis (7,8). In humans and animal models, CD8ϩ T cells are found in latently infected ganglia (9, 10). These CD8 ϩ T cells have been shown to release lytic granules containing granzyme B (GrB) in humans (9, 11) and mice (12, 13). In the setting of HSV-1 latency, rather than inducing apoptosis, GrB cleaves infected-cell polypeptide 4 (ICP4) (13), an essential viral protein needed for viral gene expression, thereby preventing viral reactivation (14). It is a wellknown clinical phenomenon that even after multiple reactivations of HSV-1 in the TG, no sensory deficits occur. Here we investigate if this observation is mirrored by the patho-anatomical findings in human TG latently infected with HSV-1.Human TG were obtained at autopsy at Ludwig Maximilians University (Munich, Germany) with the approval of the Ethics Committee of the Medical Faculty of the University (see Table S1 in the supplemental material). Whole ganglia, including neurons projecting to all three branches, were embedded directly after removal in Jung tissue freezing medium (Leica Microsystems, Nussloch, Germany). Frozen sections of 10 m were cut for immunohistochemistry and in situ hybridization (ISH), while RNA and