Immunohistochemical analysis of primary sensory neurons latently infected with herpes simplex virus type 1

We characterized the populations of primary sensory neurons that become lat ently infected with herpes simplex virus (HSV) following peripheral inocula tion. Twenty-one days after ocular inoculation with HSV strain KOS, 81% of latency-associated transcript (LAT)-positive trigeminal ganglion (TG) neuro ns coexpressed SSEA3, 71% coexpressed Trk(A) (the high-affinity nerve growt h factor receptor), and 68% coexpressed antigen recognized by monoclonal an tibody (MAb) A5; less than 5% coexpressed antigen recognized by MAb KH10. T he distribution of LAT-positive, latently infected TG neurons contrasted sh arply with (i) the overall distribution of neuronal phenotypes in latently infected TG and (ii) the neuronal distribution of viral antigen in producti vely infected TG. Similar results were obtained following ocular and footpa d inoculation with KOS/62, a LAT deletion mutant in which the LAT promoter is used to drive expression of the Escherichia coli lacZ gene. Thus, althou gh all neuronal populations within primary sensory ganglia appear to be cap able of supporting a productive infection with HSV, some neuronal phenotype s are more permissive for establishment of a latent infection with LAT expr ession than others. Furthermore, expression of HSV LAT does not appear to p lay a role in this process. These findings indicate that there are marked d ifferences in the outcome of HSV infection among the different neuronal pop ulations in the TG and highlight the key role that the host neuron may play in regulating the repertoire of viral gene expression during the establish ment of HSV latent infection.