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Gammaherpesvirinae

About: Gammaherpesvirinae is a research topic. Over the lifetime, 1233 publications have been published within this topic receiving 77581 citations.


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Journal ArticleDOI
16 Dec 1994-Science
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.
Abstract: Representational difference analysis was used to isolate unique sequences present in more than 90 percent of Kaposi's sarcoma (KS) tissues obtained from patients with acquired immunodeficiency syndrome (AIDS). These sequences were not present in tissue DNA from non-AIDS patients, but were present in 15 percent of non-KS tissue DNA samples from AIDS patients. The sequences are homologous to, but distinct from, capsid and tegument protein genes of the Gammaherpesvirinae, herpesvirus saimiri and Epstein-Barr virus. These KS-associated herpesvirus-like (KSHV) sequences appear to define a new human herpesvirus.

5,493 citations

Journal ArticleDOI
TL;DR: The Epstein–Barr virus (EBV) was discovered 36 years ago by electron microscopy of cells cultured from Burkitt's lymphoma tissue by Epstein, Achong, and Barr and has been found in tissues from other cancers, including T-cell lymphomas and Hodgkin's disease.
Abstract: The Epstein–Barr virus (EBV) was discovered 36 years ago by electron microscopy of cells cultured from Burkitt's lymphoma tissue by Epstein, Achong, and Barr.1 Four years later, in 1968, EBV was shown to be the etiologic agent of heterophile-positive infectious mononucleosis.2 EBV DNA was detected in tissues from patients with nasopharyngeal carcinoma in 1970.3 In the 1980s, EBV was found to be associated with non-Hodgkin's lymphoma and oral hairy leukoplakia in patients with the acquired immunodeficiency syndrome (AIDS).4,5 Since then, EBV DNA has been found in tissues from other cancers, including T-cell lymphomas and Hodgkin's disease.6,7 EBV is . . .

1,485 citations

Journal ArticleDOI
06 Dec 1996-Science
TL;DR: Four virus proteins similar to two human macrophage inflammatory protein (MIP) chemokines, interleukin-6 (IL-6), and interferon regulatory factor (IRF) are encoded by the Kaposi's sarcoma-associated herpesvirus (KSHV) genome.
Abstract: Four virus proteins similar to two human macrophage inflammatory protein (MIP) chemokines, interleukin-6 (IL-6), and interferon regulatory factor (IRF) are encoded by the Kaposi's sarcoma-associated herpesvirus (KSHV) genome. vIL-6 was functional in B9 proliferation assays and primarily expressed in KSHV-infected hematopoietic cells rather than KS lesions. HIV-1 transmission studies showed that vMIP-I is similar to human MIP chemokines in its ability to inhibit replication of HIV-1 strains dependent on the CCR5 co-receptor. These viral genes may form part of the response to host defenses contributing to virus-induced neoplasia and may have relevance to KSHV and HIV-I interactions.

913 citations

Journal ArticleDOI
01 Jan 1998-Nature
TL;DR: It is concluded that the KSHV G-protein-coupled receptor is a viral oncogene that can exploit cell signalling pathways to induce transformation and angiogenesis in K SHV-mediated oncogenesis.
Abstract: The Kaposi's sarcoma-associated herpesvirus (KSHV/HHV8) is a gamma-2 herpesvirus that is implicated in the pathogenesis of Kaposi's sarcoma and of primary effusion B-cell lymphomas (PELs). KSHV infects malignant and progenitor cells of Kaposi's sarcoma and PEL, it encodes putative oncogenes and genes that may cause Kaposi's sarcoma pathogenesis by stimulating angiogenesis. The G-protein-coupled receptor encoded by an open reading frame (ORF 74) of KSHV is expressed in Kaposi's sarcoma lesions and in PEL and stimulates signalling pathways linked to cell proliferation in a constitutive (agonist-independent) way. Here we show that signalling by this KSHV G-protein-coupled receptor leads to cell transformation and tumorigenicity, and induces a switch to an angiogenic phenotype mediated by vascular endothelial growth factor, an angiogenesis and Kaposi's-spindle-cell growth factor. We find that this receptor can activate two protein kinases, JNK/SAPK and p38MAPK, by triggering signalling cascades like those induced by inflammatory cytokines that are angiogenesis activators and mitogens for Kaposi's sarcoma cells and B cells. We conclude that the KSHV G-protein-coupled receptor is a viral oncogene that can exploit cell signalling pathways to induce transformation and angiogenesis in KSHV-mediated oncogenesis.

842 citations

Journal ArticleDOI
TL;DR: Using monoclonal antibody-immune microscopy, it is demonstrated that these two EBV proteins and their associated B-lymphocyte activation or adhesion molecules are expressed in the infiltrating B lymphocytes in immunocompromised patients with EBV lymphoproliferative disease.
Abstract: Epstein-Barr virus (EBV) has been associated with serious or fatal lymphoproliferative disease in immunocompromised patients. EBV nuclear protein 2 and latent membrane protein are characteristically expressed in B lymphocytes proliferating in vitro in response to growth transformation by EBV. These two proteins are thought to be effectors of lymphocyte growth since they increase the expression of B-lymphocyte activation (CD23) and cell-adhesion (LFA 3 and ICAM 1) molecules in vitro. Using monoclonal antibody-immune microscopy, we have demonstrated that these two EBV proteins and their associated B-lymphocyte activation or adhesion molecules are expressed in the infiltrating B lymphocytes in immunocompromised patients with EBV lymphoproliferative disease. These monoclonal antibodies should be useful in the early diagnosis of EBV lymphoproliferative disease and in distinguishing it from other B-lymphocyte cancers associated with EBV, such as Burkitt's lymphoma. The finding of EBV nuclear protein 2 and latent membrane protein and their associated activation or adhesion molecules provides a further pathophysiologic link between EBV and the proliferation of B lymphocytes in immunocompromised patients.

782 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20235
20228
20211
20203
20194
20184