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Review
. 2010 Jul 22;8(1):100-15.
doi: 10.1016/j.chom.2010.06.014.

Viral latency and its regulation: lessons from the gamma-herpesviruses

Samuel H Speck  1 , Don Ganem
Affiliations
Review

Viral latency and its regulation: lessons from the gamma-herpesviruses

Samuel H Speck et al. Cell Host Microbe. .

Abstract

Latency is a state of cryptic viral infection associated with genomic persistence and highly restricted gene expression. Its hallmark is reversibility: under appropriate circumstances, expression of the entire viral genome can be induced, resulting in the production of infectious progeny. Among the small number of virus families capable of authentic latency, the herpesviruses stand out for their ability to produce such infections in every infected individual and for being completely dependent upon latency as a mode of persistence. Here, we review the molecular basis of latency, with special attention to the gamma-herpesviruses, in which the understanding of this process is most advanced.

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Figures

Figure 1
Figure 1
Schematic illustration of EBV EBNA and LMP gene transcription, and auto-regulation of viral latency-associated gene expression by the EBNA gene products. An exploded view of Cp- and Wp –driven EBNA gene transcription is shown, depicting the organization of exons immediately downstream of each promoter. Cp-initiated transcript contain 2 unique exons, C1 and C2, which splice to a variable number of W1 and W2 exons encoded within the 3.0Kb internal repeats. Wp-initiated transcript contain a single unique exon, W0, which splices to a variable number of W1 and W2 repeat exons. See text for additional details regarding EBV gene expression during different stages of infection. Also shown in the inset is the predicted membrane topology of the LMP-1 and LMP-2a proteins, along with known cellular interacting partners and signaling pathways activated by these proteins.
Figure 2
Figure 2
Model depicting the different EBV latency programs expressed during the progression of infected naïve B cells through a germinal center reaction and establishment of latency in memory B cells. Also shown is virus reactivation linked to plasma cell differentiation. See text for additional details.
Figure 3
Figure 3
Major latency locus of KSHV. Top line: major ORFS of the locus. ORF-73 encodes LANA; ORF-72 encodes v-cyclin (v-CYC); ORF-71 encodes v-FLIP; ORF-K12 encodes kaposin A; DRs 1 and 2 encode direct repeats in which translation of kaposins B and C initiate. LIR, long interspersed repeats of unknown function. Middle panel: KSHV microRNA (miR) cluster, with pre-miRNAs indicated by arrowheads. Bottom panels: Structures of mRNAs directed by the kaposin (or LTd) promoter and by the LANA (or LTc) promoter. Figure modified with permission from Ganem (2010) J Clin Invest, in press.
Figure 4
Figure 4
Alignment of the MHV68 and KSHV genomes, depicting the large blocks of conserved genes interspersed with genes unique to each virus (K genes for KSHV - exception, K3 and K5 which are homologous the K3 gene in MHV68 - and M gene for MHV68). Shown below is data compiled from two independent transposon mutagenesis screens of the MHV68 genome, which identified genes involved in virus replication in permissive fibroblasts. Red arrow depict genes essential for replication, while orange arrows depict genes the play an important role in replication but are not essential. Green arrows depict genes that are dispensable for virus replication in tissue culture.
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