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]