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Open AccessJournal ArticleDOI

Mechanisms of Kaposi's Sarcoma-Associated Herpesvirus Latency and Reactivation

TLDR
The cellular and molecular basis of Kaposi's sarcoma-associated herpesvirus latency and reactivation is reviewed with a focus on the most recent advancements in the field.
Abstract
The life cycle of Kaposi's sarcoma-associated herpesvirus (KSHV) consists of latent and lytic replication phases. During latent infection, only a limited number of KSHV genes are expressed. However, this phase of replication is essential for persistent infection, evasion of host immune response, and induction of KSHV-related malignancies. KSHV reactivation from latency produces a wide range of viral products and infectious virions. The resulting de novo infection and viral lytic products modulate diverse cellular pathways and stromal microenvironment, which promote the development of Kaposi's sarcoma (KS). The mechanisms controlling KSHV latency and reactivation are complex, involving both viral and host factors, and are modulated by diverse environmental factors. Here, we review the cellular and molecular basis of KSHV latency and reactivation with a focus on the most recent advancements in the field.

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Cis and Trans Acting Factors Involved in Human Cytomegalovirus Experimental and Natural Latent Infection of CD14 (+) Monocytes and CD34 (+) Cells

TL;DR: Next generation sequencing deduced the transcriptome of HCMV latently infected CD14 (+) and CD34 (+) cells in experimental as well as natural latency settings and showed that the terminal repeat (TR) region of the latent viral genome is depleted of nucleosomes suggesting that this region may contain an element mediating viral genome maintenance.
Journal ArticleDOI

Anti-herpesvirus treatment and risk of Kaposi's sarcoma in HIV infection.

TL;DR: In this paper, the authors investigated the association between use of anti-herpesvirus drugs and Kaposi's sarcoma in a large unselected group of patients with AIDS.
Journal ArticleDOI

KSHV LANA--the master regulator of KSHV latency.

TL;DR: The newly annotated latent genes and the role of major latent proteins in KSHV biology are discussed, including LANA, which is among the most abundantly expressed proteins during latency and is required for various nuclear functions including the recruitment of cellular machineries for viral DNA replication and segregation of the replicated genomes to daughter cells.
Journal ArticleDOI

Molecular Biology of KSHV Lytic Reactivation

TL;DR: Some of the pivotal genetic and epigenetic factors that control KSHV reactivation from the transcriptionally restricted latent program are discussed.
References
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Journal ArticleDOI

Identification of herpesvirus-like DNA sequences in AIDS-associated Kaposi's sarcoma

TL;DR: unique sequences present in more than 90 percent of Kaposi's sarcoma tissues obtained from patients with acquired immunodeficiency syndrome (AIDS) appear to define a new human herpesvirus.
Journal ArticleDOI

Kaposi's Sarcoma–Associated Herpesvirus-Like DNA Sequences in AIDS-Related Body-Cavity–Based Lymphomas

TL;DR: A high degree of conservation of KSHV sequences in Kaposi's sarcoma and in the eight lymphomas suggests the presence of the same agent in both lesions, suggesting that a novel herpesvirus has a pathogenic role in AIDS-related body-cavity-based lymphomas.
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Kaposi's sarcoma-associated herpesvirus-like DNA sequences in multicentric Castleman's disease

TL;DR: Data suggest that KSHV could play a role in the pathogenesis of MCD, especially in HIV-infected patients, which is a close association with Kaposi's sarcoma.
Journal ArticleDOI

Viral FLICE-inhibitory proteins (FLIPs) prevent apoptosis induced by death receptors

TL;DR: A new family of viral inhibitors (v-FLIPs) which interfere with apoptosis signalled through death receptors3 and which are present in several γ-herpesviruses (including Kaposi's-sarcoma-associated human herpesvirus-8), as well as in the tumorigenic human molluscipoxvirus4.
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