Varicella-zoster virus (VZV) causes
chickenpox, establishes latency in trigeminal (TG) and dorsal root ganglia (DRG), and can lead to
herpes zoster upon reactivation. The VZV
proteome expressed during latency remains ill-defined, and previous studies have shown discordant data on the spectrum and expression pattern of VZV
proteins and transcripts in latently infected human ganglia. Recently, Zerboni and colleagues have provided new insight into this discrepancy (Zerboni et al. in J Virol 86:578-583, 2012). They showed that VZV-specific
ascites-derived
monoclonal antibody (mAb) preparations contain endogenous
antibodies directed against
blood group A1
proteins, resulting in false-positive intra-neuronal VZV staining in
formalin-fixed human DRG. The aim of the present study was to confirm and extend this phenomenon to snap-frozen TG (
n=30) and DRG (n=9) specimens of
blood group genotyped donors (
n=30). The number of immunohistochemically stained neurons was higher with mAb directed to immediate early
protein 62 (IE62) compared with IE63. The IE63 mAb-positive neurons always co-stained for IE62 but not vice versa. The mAb staining was confined to distinct large intra-neuronal vacuoles and restricted to A1(POS) donors. Anti-VZV mAb staining in neurons, but not in VZV-infected cell monolayers, was obliterated after mAb adsorption against
blood group A1 erythrocytes. The data presented demonstrate that neuronal VZV
protein expression detected by
ascites-derived mAb in snap-frozen TG and DRG of
blood group A1(POS) donors can be misinterpreted due to the presence of endogenous
antibodies directed against
blood group A1-associated
antigens present in
ascites-derived VZV-specific mAb preparations.