Classic Kaposi sarcoma

Iscovich, José; Boffetta, Paolo; Franceschi, Silvia; Azizi, Esther; Sarid, Ronit

doi:10.1002/(sici)1097-0142(20000201)88:3<500::aid-cncr3>3.0.co;2-9

Cited by 209 publications

(69 citation statements)

References 173 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Classic KS occurs as a rare and indolent form in elderly Mediterranean men, with particularly high incidence in Italy, Greece, Turkey, and Israel (230,452). Historically, KS incidence in the Mediterranean is up to 10-fold higher than in the rest of Europe and the United States (40,133,204).…”

Section: Classic Ksmentioning

confidence: 99%

“…The high frequency of iatrogenic KS in Saudi Arabia reflects the 7% endemic seroprevalence of KSHV in healthy Saudi donors or patients with non-KS malignancies (412). Interestingly, transplant-associated KS is seen predominantly in kidney allograft recipients and not other solid-organ or bone marrow transplant recipients (230); kidney recipients have a greater than two-fold-higher seroprevalence than those at low risk of KS in France (85). Although Andreoni et al found that 21.4% of liver recipients, but only 8.6% of kidney recipients, seroconverted for KSHV, the risk of KS was higher in the kidney transplant recipients.…”

Section: Iatrogenic Ksmentioning

confidence: 99%

See 1 more Smart Citation

Molecular Genetics of Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8) Epidemiology and Pathogenesis

Dourmishev

Palmeri

et al. 2003

Microbiol Mol Biol Rev

309

371

View full text Add to dashboard Cite

Kaposi's sarcoma had been recognized as unique human cancer for a century before it manifested as an AIDS-defining illness with a suspected infectious etiology. The discovery of Kaposi's sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus-8, in 1994 by using representational difference analysis, a subtractive method previously employed for cloning differences in human genomic DNA, was a fitting harbinger for the powerful bioinformatic approaches since employed to understand its pathogenesis in KS. Indeed, the discovery of KSHV was rapidly followed by publication of its complete sequence, which revealed that the virus had coopted a wide armamentarium of human genes; in the short time since then, the functions of many of these viral gene variants in cell growth control, signaling apoptosis, angiogenesis, and immunomodulation have been characterized. This critical literature review explores the pathogenic potential of these genes within the framework of current knowledge of the basic herpesvirology of KSHV, including the relationships between viral genotypic variation and the four clinicoepidemiologic forms of Kaposi's sarcoma, current viral detection methods and their utility, primary infection by KSHV, tissue culture and animal models of latent- and lytic-cycle gene expression and pathogenesis, and viral reactivation from latency. Recent advances in models of de novo endothelial infection, microarray analyses of the host response to infection, receptor identification, and cloning of full-length, infectious KSHV genomic DNA promise to reveal key molecular mechanisms of the candidate pathogeneic genes when expressed in the context of viral infection

show abstract

Section: Classic Ksmentioning

confidence: 99%

Section: Iatrogenic Ksmentioning

confidence: 99%

Molecular Genetics of Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8) Epidemiology and Pathogenesis

Dourmishev

Palmeri

et al. 2003

Microbiol Mol Biol Rev

309

371

View full text Add to dashboard Cite

show abstract

“…HHV-8 DNA has been detected in 95% of HIV-associated KS, classical KS, and endemic KS (33,134,135,257,258,262,263). The DNA from either fresh or frozen KS samples can be detected by PCR after 30 to 35 amplifications (Fig.…”

Section: Nucleic Acidsmentioning

confidence: 99%

Spectrum of Kaposi's Sarcoma-Associated Herpesvirus, or Human Herpesvirus 8, Diseases

Ablashi¹,

Chatlynne²,

Whitman³

et al. 2002

Clin Microbiol Rev

275

182

View full text Add to dashboard Cite

Human herpesvirus 8 (HHV-8), also known as Kaposi's sarcoma-associated herpesvirus (KSHV), discovered in 1994, is a human rhadinovirus (gamma-2 herpesvirus). Unlike other human herpesviruses (herpes simplex virus, Epstein-Barr virus, varicella-zoster virus, cytomegalovirus, HHV-6, and HHV-7), it is not widespread in the general population and has many unique proteins. HHV-8 is strongly associated with all subtypes of Kaposi's sarcoma (KS), multicentric Castleman's disease, and a rare form of B-cell lymphoma, primary effusion lymphoma. In addition, HHV-8 DNA sequences have been found in association with other diseases, but the role of the virus in these diseases is largely unconfirmed and remains controversial. The seroprevalence of HHV-8, based on detection of latent and lytic proteins, is 2 to 5% in healthy donors except in certain geographic areas where the virus is endemic, 80 to 95% in classic KS patients, and 40 to 50% in HIV-1 patients without KS. This virus can be transmitted both sexually and through body fluids (e.g., saliva and blood). HHV-8 is a transforming virus, as evidenced by its presence in human malignancies, by the in vitro transforming properties of several of its viral genes, and by its ability to transform some primary cells in culture. It is not, however, sufficient for transformation, and other cofactors such as immunosuppressive cytokines are involved in the development of HHV-8-associated malignancies. In this article, we review the biology, molecular virology, epidemiology, transmission, detection methods, pathogenesis, and antiviral therapy of this newly discovered human herpesvirus

show abstract

“…As the etiologic agent for KS, HHV8 generally results in latent infection in its natural host cells (14). Based on several extensive studies on the association of HIV and the development of KS, it is now understood that HHV8 is required but not necessarily sufficient for the development of KS (15). In fact, the incidence rate of KS among HIV-1-infected individuals is up to 100,000-fold higher than that among the general population, and 300-fold higher than that for persons with other types of acquired immunosuppression.…”

mentioning

confidence: 99%

Reciprocal Regulatory Interaction between Human Herpesvirus 8 and Human Immunodeficiency Virus Type 1

Huang

Chao

Chen

et al. 2001

Journal of Biological Chemistry

View full text Add to dashboard Cite

Human herpesvirus 8 (HHV8) is the primary viral etiologic agent in Kaposi's sarcoma (KS). However, individuals dually infected with both HHV8 and human immunodeficiency virus type 1 (HIV-1) show an enhanced prevalence of KS when compared with those singularly infected with HHV8. Host immune suppression conferred by HIV infection cannot wholly explain this increased presentation of KS. To better understand how HHV8 and HIV-1 might interact directly in the pathogenesis of KS, we queried for potential regulatory interactions between the two viruses. Here, we report that HHV8 and HIV-1 reciprocally up-regulate the gene expression of each other. We found that the KIE2 immediate-early gene product of HHV8 interacted synergistically with Tat in activating expression from the HIV-1 long terminal repeat. On the other hand, HIV-1 encoded Tat and Vpr proteins increased intracellular HHV8-specific expression. These results provide molecular insights correlating coinfection with HHV8 and HIV-1 with an unusually high incidence of KS.

show abstract

Classic Kaposi sarcoma

Cited by 209 publications

References 173 publications

Molecular Genetics of Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8) Epidemiology and Pathogenesis

Molecular Genetics of Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8) Epidemiology and Pathogenesis

Spectrum of Kaposi's Sarcoma-Associated Herpesvirus, or Human Herpesvirus 8, Diseases

Reciprocal Regulatory Interaction between Human Herpesvirus 8 and Human Immunodeficiency Virus Type 1

Contact Info

Product

Resources

About