Human herpesvirus 8 – A novel human pathogen

Edelman, Daniel C.

doi:10.1186/1743-422x-2-78

Cited by 83 publications

(41 citation statements)

References 293 publications

(452 reference statements)

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“…Following the primary infection, HHV8 establishes life-long latency in B-cells. During latency, no viral particles are produced, but a set of viral genes that promote cellular proliferation are expressed, which enable the virus to perpetuate in the host B-cell population 13,19. Cytotoxic T-cells normally limit this virally driven cellular proliferation by recognizing viral proteins.…”

Section: Etiology and Pathogenesismentioning

confidence: 99%

Current Concepts in Primary Effusion Lymphoma and Other Effusion-Based Lymphomas

et al. 2014

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Primary effusion lymphoma (PEL) is a human herpes virus 8 (HHV8)-positive large B-cell neoplasm that presents as an effusion with no detectable tumor in individuals with human immunodeficiency virus infection or other immune deficiencies. PEL is an aggressive neoplasm with a poor prognosis. PEL cells show diverse morphologies, ranging from immunoblastic or plasmablastic to anaplastic. The immunophenotype of PEL is distinct, but its lineage can be misdiagnosed if not assessed thoroughly. PEL cells usually express CD45, lack B- and T-cell-associated antigens, and characteristically express lymphocyte activation antigens and plasma cell-associated antigens. Diagnosis of PEL often requires the demonstration of a B-cell genotype. HHV8 must be detected in cells to diagnose PEL. In most cases, PEL cells also harbor the Epstein-Barr virus (EBV) genome. Similar conditions associated with HHV8 but not effusion-based are called "extracavitary PELs." PELs should be differentiated from HHV8-negative, EBV-positive, body cavity-based lymphomas in patients with long-standing chronic inflammation; the latter can occur in tuberculous pleuritis, artificial pneumothorax, chronic liver disease and various other conditions. Despite their morphological similarity, these various lymphomas require different therapeutic strategies and have different prognostic implications. Correct diagnosis is essential to manage and predict the outcome of patients with PEL and related disorders.

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Section: Etiology and Pathogenesismentioning

confidence: 99%

Current Concepts in Primary Effusion Lymphoma and Other Effusion-Based Lymphomas

et al. 2014

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“…KSHV is known to be the causative agent of Kaposi sarcoma, as well as of PEL and some types of multicentric Castleman's disease (reviewed in [100]). ICN1 is aberrantly accumulated in KSHV latently infected PEL cells [101][102][103].…”

Section: Virus-associated B-cell Lymphomasmentioning

confidence: 99%

Notch Signaling in Leukemias and Lymphomas

Jundt¹,

Schwarzer²,

Dörken

2008

CMM

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Aberrant Notch activation is linked to cancer since 1991 when mammalian Notch1 was first identified as part of the translocation t(7;9) in a subset of human T-cell acute lymphoblastic leukemias (T-ALL). Since then oncogenic Notch signaling has been found in many solid and hematopoietic neoplasms. Depending on tumor type Notch interferes with differentiation, proliferation, survival, cell-cycle progression, angiogenesis, and possibly self-renewal. In hematopoietic neoplasms, recent findings indicate an important role of Notch for T-ALL induction and progression and the pathogenesis of human T- and B-cell-derived lymphomas. Notch signaling has been identified as a potential new therapeutic target in these hematopoietic neoplasms. This review will focus on the most recent findings on Notch signaling in leukemias and lymphomas and its potential role in the maintenance of malignant stem cells.

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“…The incidence of KS in HIV-infected individuals in the United States has been decreasing steadily due to the implementation of antiretroviral therapy 4,7 . However, it retains a high morbidity and mortality in AIDS patients with disseminated disease and some sub-Saharan African countries 6,8,9 .…”

Section: Introductionmentioning

confidence: 99%

Kaposi sarcoma-associated herpesvirus promotes tumorigenesis by modulating the Hippo pathway

Liu

Kim

et al. 2014

Oncogene

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Kaposi sarcoma-associated herpesvirus (KSHV) is an oncogenic virus and the culprit behind the human disease Kaposi sarcoma (KS), an AIDS-defining malignancy. KSHV encodes a viral G-protein-coupled receptor (vGPCR) critical for the initiation and progression of KS. In this study, we identified that YAP/TAZ, two homologous oncoproteins inhibited by the Hippo tumor suppressor pathway, are activated in KSHV infected cells in vitro, KS-like mouse tumors, and clinical human KS specimens. The KSHV-encoded vGPCR acts through Gq/11 and G12/13 to inhibit the Hippo pathway kinases Lats1/2, promoting the activation of YAP/TAZ. Furthermore, depletion of YAP/TAZ blocks vGPCR-induced cell proliferation and tumorigenesis in a xenograft mouse model. The vGPCR-transformed cells are sensitive to pharmacological inhibition of YAP. Our study establishes a pivotal role of the Hippo pathway in mediating the oncogenic activity of KSHV and development of KS, and also suggests a potential of using YAP inhibitors for KS intervention.

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Human herpesvirus 8 – A novel human pathogen

Cited by 83 publications

References 293 publications

Current Concepts in Primary Effusion Lymphoma and Other Effusion-Based Lymphomas

Current Concepts in Primary Effusion Lymphoma and Other Effusion-Based Lymphomas

Notch Signaling in Leukemias and Lymphomas

Kaposi sarcoma-associated herpesvirus promotes tumorigenesis by modulating the Hippo pathway

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