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

Ablashi, Dharam V.; Chatlynne, Louise G.; Whitman, James E.; Cesarman, Ethel

doi:10.1128/cmr.15.3.439-464.2002

Cited by 275 publications

(213 citation statements)

References 277 publications

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“…Possible causes of such associations are outlined in a number of reviews [6,10,12,29] and reports relating to the specific entities, that is, Kaposi's sarcoma [9,30], PNP [31], POEMS [29], and lymphoma [30,[32][33][34][35].…”

Section: Discussionmentioning

confidence: 99%

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Castleman's Disease: Systematic Analysis of 416 Patients from the Literature

2011

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Learning Objectives After completing this course, the reader will be able to: Describe the centricity and histopathology profiles of each of the three classes of HIV‐negative patients identified in this analysis. Correlate nosological classification and outcomes in patients with Castleman's disease. This article is available for continuing medical education credit at http://CME.TheOncologist.com Background. Castleman's disease is a rare primary disease of the lymph nodes with limited available clinical information. Methods. A systematic literature search identified 416 cases amenable to detailed analysis. Results. In HIV− patients, centricity, pathology type, the presence of symptoms, gender, and age all predict outcome in univariate analyses. The 3‐year disease‐free survival (DFS) rate for patients with unicentric hyaline vascular disease (49.5% of cases, class I) was 92.5%, versus 45.7% for those with multicentric plasma cell disease (20.2% of cases, class III) and 78.0% for those with any other combination (22.6% of cases, class II) (p < .0001). HIV+ patients (class IV) exclusively presented with multicentric plasma cell disease and had a 3‐year DFS rate of only 27.8%. Kaposi's sarcoma and lymphoma were observed in 59.3% and 9.4% of HIV+ patients and in 2.6% and 3.6% of HIV− patients (p < .0001). Paraneoplastic pemphigus and the syndrome of polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes were observed exclusively in HIV− patients at a rate of 1.3% and 1.8%, respectively. Conclusion. Clinical, pathological, and viral markers allow for the classification of Castleman's disease into groups with markedly different outcomes and disease associations.

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Section: Discussionmentioning

confidence: 99%

“…A number of excellent reviews are available and give general oversight [3][4][5][6][7][8][9], focus on pathogenesis [4,10], pathological features [11,12], clinical presentation in HIV Ϫ [13] and HIV ϩ [14,15] patients, and management aspects [8,16,17].…”

Section: Introductionmentioning

confidence: 99%

Castleman's Disease: Systematic Analysis of 416 Patients from the Literature

2011

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“…13,38 PEL cells are always infected with a transforming human g herpes virus (HHV) called Kaposi's sarcoma herpes virus (KSHV/HHV8) and often co-infected with EBV. 41 These cells, which have a latency I phenotype, as well as EBV(À) PEL cells are very sensitive to nutlin-3-induced apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Activation of p53 by MDM2 antagonists has differential apoptotic effects on Epstein–Barr virus (EBV)-positive and EBV-negative Burkitt's lymphoma cells

et al. 2009

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p53 inactivation is often observed in Burkitt's lymphoma (BL) cells, because of either mutations in p53 gene or an overexpression of the p53-negative regulator MDM2. Epstein-Barr virus (EBV) is present in virtually 100% of BL cases occurring in endemic areas, but in only 10-20% of sporadic cases. In EBV(À) BL cells, reactivation of p53, induced by reducing MDM2 protein level, led to apoptosis. We show here that nutlin-3, a potent antagonist of MDM2, activates the p53 pathway in all BL cell lines harboring wild-type p53, regardless of EBV status. However, nutlin-3 strongly induced apoptosis in EBV(À) or latency I EBV( þ ) cells, whereas latency III EBV( þ ) cells were much more resistant. Prior treatment with sublethal doses of nutlin-3 sensitizes EBV(À) or latency I EBV( þ ) cells to apoptosis induced by etoposide or melphalan, but protects latency III EBV( þ ) cells. p21 WAF1 which is overexpressed in the latter, is involved in this protective effect, as siRNA-mediated inhibition of p21 WAF1 restores sensitivity to etoposide. Nutlin-3 protects latency III BL cells by inducing a p21 WAF1 -mediated G1 arrest. Most BL patients with wild-type p53 tumors could therefore benefit from treatment with nutlin-3, after a careful determination of the latency pattern of EBV in infected patients.

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“…A possible source of nonsexual horizontal transmission (e.g., through saliva) was suggested by a study that analyzed KSHV transmission in children before puberty (38). KSHV transmission by injection drug use was rare among drug users in Amsterdam (39), but another study demonstrated that KSHV seropositivity increased in association with injection drug use (40).…”

Section: Discussionmentioning

confidence: 99%

Kaposi's sarcoma-associated herpesvirus infection and Kaposi's sarcoma in Brazil

Silva

Oliveira

Borges

et al. 2006

Braz J Med Biol Res

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Kaposi's sarcoma (KS) became a critical health issue with the emergence of acquired immunodeficiency syndrome (AIDS) in the 1980s. Four clinical-epidemiological forms of KS have been described: classical KS, endemic KS, iatrogenic KS, and AIDS-associated KS. In 1994, Kaposi's sarcoma-associated herpesvirus (KSHV) or human herpesvirus type 8 was identified by Chang and colleagues, and has been detected worldwide at frequencies ranging from 80 to 100%. The aim of the present study was to evaluate the frequency of KSHV infection in KS lesions from HIV-positive and HIV-negative patients in Brazil, as well as to review the current knowledge about KS transmission and detection. For these purposes, DNA from 51 cases of KS was assessed by PCR: 20 (39.2%) cases of classical KS, 29 (56.9%) of AIDS-associated KS and 2 (3.9%) of iatrogenic KS. Most patients were males (7.5:1, M/F), and mean age was 47.9 years (SD = ± 18.7 years). As expected, HIV-positive KS patients were younger than patients with classical KS. On the other hand, patients with AIDS-associated KS have early lesions (patch and plaque) compared to classical KS patients (predominantly nodular lesions). This is assumed to be the result of the early diagnose of KS in the HIVpositive setting. KSHV infection was detected by PCR in almost all cases (48/51; 94.1%), irrespectively of the clinical-epidemiological form of KS. These results show that KSHV is associated with all forms of KS in Brazilian patients, a fact that supports the role of this virus in KS pathogenesis. Correspondence

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

Cited by 275 publications

References 277 publications

Castleman's Disease: Systematic Analysis of 416 Patients from the Literature

Castleman's Disease: Systematic Analysis of 416 Patients from the Literature

Activation of p53 by MDM2 antagonists has differential apoptotic effects on Epstein–Barr virus (EBV)-positive and EBV-negative Burkitt's lymphoma cells

Kaposi's sarcoma-associated herpesvirus infection and Kaposi's sarcoma in Brazil

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