Abstract
Latency establishment is the hallmark feature of herpesviruses, a group of viruses, of which nine are known to infect humans. They have co-evolved alongside their hosts, and mastered manipulation of cellular pathways and tweaking various processes to their advantage. As a result, they are very well adapted to persistence. The members of the three subfamilies belonging to the family Herpesviridae differ with regard to cell tropism, target cells for the latent reservoir, and characteristics of the infection. The mechanisms governing the latent state also seem quite different. Our knowledge about latency is most complete for the gammaherpesviruses due to previously missing adequate latency models for the alpha and beta-herpesviruses. Nevertheless, with advances in cell biology and the availability of appropriate cell-culture and animal models, the common features of the latency in the different subfamilies began to emerge. Three criteria have been set forth to define latency and differentiate it from persistent or abortive infection: 1) persistence of the viral genome, 2) limited viral gene expression with no viral particle production, and 3) the ability to reactivate to a lytic cycle. This review discusses these criteria for each of the subfamilies and highlights the common strategies adopted by herpesviruses to establish latency.
Highlights
Herpesviruses are a family of enveloped viruses with large double-stranded DNA genomes [1].Their life cycle is characterized by two phases: the lytic cycle—when the virus is actively replicating and the latency, which enables these viruses to persist for the lifetime of the host
These three criteria set latency apart from a persistent infection, during which new viral particles are produced; and abortive infection, in which the virus is unable to reactivate [1]. The name of this virus family derives from the Greek word herpes and originally referred to the spreading lesions observed during herpes simplex virus (HSV) or varicella zoster virus (VZV) infection [3], but it could refer to the quiescent nature of herpesviral infections, since latency is the hallmark of their life cycle
The common feature for all herpesviruses is the persistence of the genome in form of an episome, the difference with regards to persistence lies in that the beta- and gammaherpesviruses, encode a protein participating in latent replication and genome tethering, and alphaherpesviruses, do not have such a protein, as they persist in non-dividing neurons
Summary
Herpesviruses are a family of enveloped viruses with large double-stranded DNA genomes [1]. The Betaherpesvirinae include the human cytomegalovirus (HCMV), human herpesvirus 6A and B (HHV-6A and B), and human herpesvirus 7 (HHV-7) and have species-specific tropism and a longer (days) replication cycle [6] They spread slower and the infection results in characteristic cell enlargement [3,7]. The Gammaherpesvirinae, which include Epstein–Barr virus (EBV) and Kaposi’s sarcoma-associated herpesvirus (KSHV), have very narrow tropism both with regard to the host and the cell type, they are species-specific and infect lymphocytes, epithelial and endothelial cells, and establish latency in B lymphocytes. KSHV is the causative agent of Kaposi sarcoma (KS), plasmablastic variant of Multicentric Castleman’s disease (MCD) and primary effusion lymphoma (PEL) [12] Both of the viruses induce tumor formation through persistence of the viral genome and continuous expression of viral latent proteins (see below), which have the ability to inhibit apoptosis, evade anti-viral immune response, and induce proliferation [13]
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