Latency mechanism | Latency establishment | Reactivation | HSV strain and ref. |
Chromatin modification leads to lytic gene silencing and expression of LATs and miRNA. | HSV infection at the distal axon, retrograde to neuronal nucleus. | LAT induces efficient reactivation. | HSV-1-KOS/62/17/ McKrae [44] |
In sensory neurons, HSV genome remains nonreplicative and viral genes are silenced except LAT. | LAT deletion analysis indicated that LAT enhances the latency establishment. | Fever, stress, and UV irradiation or abrasion. | HSV-1-17/F [51] |
LAT is able to play an indispensable role in the establishment of incubation period via reducing mRNA levels of IE gene. | LAT inhibits viral replication in nerve cells | LAT enables HSV reactivation. | HSV-1-F/KOS [46] |
HSV virions are transported to the cell body within the TG to suppress effectively lytic genes. | When the virus cleavage gene is suppressed, the HSV genome enters a nucleosomal associated latent state without DNA replication in the sensory ganglia. | A stress stimulus. | HSV-1-17/KOS [48] |
ICP0 promoted histones and heterochromatin modifications to silence lytic gene expression. | ICP0 promoted the establishment of latency. | ICP0 accelerates the expression of LAT and lytic genes in latent infected ganglia. | HSV-1-KOS [49] |