Figure 3

Model of TR/TH-mediated HSV-1 latency and reactivation. The working hypothesis is that liganded TR repressed the transcription of TK in neurons, leading to inhibition of viral replication and α expression thus promoted the condition for latency. Transient or chronic hypothyroidism reduced the TH level and the shortage of hormone decreased the repression of TK and ICP0, therefore increased the viral replication, gene expression, and release of infectious viruses. All of these led to viral reactivation.