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Open AccessJournal ArticleDOI

Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8)

Thomas F. Schulz
- 01 Jul 1998 - 
- Vol. 79, Iss: 7, pp 1573-1591
TLDR
The unique epidemiology of KSHV and its public health importance, especially to parts of sub-Saharan Africa, suggest that this virus be accorded an important priority in the development of techniques for its control and treatment.
Abstract
As epidemiologic evidence accumulates, it is becoming increasingly clear that Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) (or human herpesvirus 8 [HHV-8]) is the likely infectious cause of KS and related neoplastic disorders. Immunosuppression is an important cofactor in KS pathogenesis, as shown by the occurrence of KS in post-transplant patients and its occasional regression after the reduction of iatrogenic immunosuppression. Whether KS is a hyperplastic process driven by cytokine dysregulation or represents the oligo-or monoclonal-expansion of virus-transformed endothelial cells remains controversial. Near-universal detection of KSKSHV DNA in all of the histologically indistinguishable forms of KS suggests that they share a common etiology. In addition to studies suggesting persistence of KSHV in prostate tissues from KS patients, one study has found that dorsal root ganglia may harbor viral DNA in patients with AIDS-KS. Cultivation of the virus in cells uninfected with Epstein-Barr virus (EBV) has led to the development of serologic tests and studies of KSHV gene expression during latency and lytic replication. The close correspondence between signal pathways activated by EBV infection and those activated by virus-encoded homologs during KSHV infection is seen for interleukin-6 (IL-6) signal transduction. DNA tumor viruses have been essential tools in dissecting out transformation pathways, and KSHV promises to provide a unique model for investigating virus-induced transformation. The unique epidemiology of KSHV and its public health importance, especially to parts of sub-Saharan Africa, suggest that this virus be accorded an important priority in the development of techniques for its control and treatment.

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Citations
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Journal ArticleDOI

Downregulation of major histocompatibility complex class I molecules by Kaposi's sarcoma-associated herpesvirus K3 and K5 proteins

TL;DR: Results demonstrate that Kaposi's sarcoma-associated herpesvirus has evolved a novel immune evasion mechanism by harboring similar but distinct genes, K3 and K5, which target MHC class I molecules in different ways.
Journal ArticleDOI

Reactivation of Kaposi's Sarcoma-Associated Herpesvirus Infection from Latency by Expression of the ORF 50 Transactivator, a Homolog of the EBV R Protein☆

TL;DR: It is shown that deregulated expression of a single viral gene, ORF 50, which encodes a transactivator able to selectively upregulate delayed-early viral genes, suffices to disrupt latency and induce the lytic gene cascade in latently infected B cells.
Journal ArticleDOI

Transcriptional Activation by the Product of Open Reading Frame 50 of Kaposi’s Sarcoma-Associated Herpesvirus Is Required for Lytic Viral Reactivation in B Cells

TL;DR: Results indicate that the ORF50 gene product plays an essential role in KSHV lytic replication and are consistent with its action as a putative molecular switch controlling the induction of virus from latency.
Journal ArticleDOI

Integrin α3β1 (CD 49c/29) Is a Cellular Receptor for Kaposi's Sarcoma-Associated Herpesvirus (KSHV/HHV-8) Entry into the Target Cells

TL;DR: Human herpesvirus-8 infection induced the integrin-mediated activation of focal adhesion kinase (FAK) and a role for α3β1 integrin and the associated signaling pathways in HHV-8 entry into the target cells is implicated.
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Viral carcinogenesis: revelation of molecular mechanisms and etiology of human disease.

TL;DR: Viruses are now accepted as bona fide etiologic factors of human cancer; these include hepatitis B virus, Epstein-Barr virus, human papillomaviruses, human T-cell leukemia virus type I and hepatitis C virus, plus several candidate human cancer viruses.
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Journal ArticleDOI

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

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Journal ArticleDOI

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Journal ArticleDOI

Identification of RANTES, MIP-1α, and MIP-1β as the Major HIV-Suppressive Factors Produced by CD8+ T Cells

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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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