Maintenance of herpesvirus latency. A. HSV-1. Viral latency associated transcripts (LAT) encode micro RNAs (miRNA) that suppress the expression of viral IE proteins. Nerve growth factor (NGF) induced signaling also helps maintain latency in vitro. Non-dividing neurons do not require a mechanism to replicate or faithfully partition viral genomes. B. HCMV. The contributions of viral mRNAs/transcripts detected during latency (CTLs, LUNA, UL138, US28, vIL10) to the establishment, maintenance, animation, or reactivation from latency have not been fully characterized. Whether or not latently infected progenitor cells divide or self-renew (arrow with question mark) is not known, thus the need for (or presence of) replication or partition functions is also unclear. C. EBV. The viral EBNA1 protein provides replication and partition functions required to maintain latency in dividing B cells. Different types of EBV latency also express other latent genes whose functions appear to be proliferation induction, apoptosis inhibition and immune evasion. EBER and BART transcripts are also expressed during latency. EBERs inhibit protein kinase R (PKR) to maintain translational proficiency, and BARTs are processed into miRNAs. Viral genome methylation prohibits lytic phase gene expression.