Multiple Epstein-Barr virus-associated subcutaneous angioleiomyomas in a patient with acquired immunodeficiency syndrome

2002 ◽  
Vol 147 (3) ◽  
pp. 563-567 ◽  
Author(s):  
J.Y-F. Chang ◽  
C-S. Wang ◽  
C-C. Hung ◽  
T-F. Tsai ◽  
C-H. Hsiao
Keyword(s):  
Acquired Immunodeficiency Syndrome ◽  
Epstein Barr Virus ◽  
Barr Virus ◽  
Acquired Immunodeficiency ◽  
Epstein Barr ◽  
Immunodeficiency Syndrome

scholarly journals Epstein-Barr virus infection precedes clonal expansion in Burkitt's and acquired immunodeficiency syndrome-associated lymphoma [see comments]

Blood ◽  
1991 ◽  
Vol 77 (5) ◽  
pp. 1092-1095 ◽  
Author(s):  
A Neri ◽  
F Barriga ◽  
G Inghirami ◽  
DM Knowles ◽  
J Neequaye ◽  
...  
Keyword(s):  
Acquired Immunodeficiency Syndrome ◽  
Epstein Barr Virus ◽  
Clonal Expansion ◽  
Epstein Barr Virus Infection ◽  
Barr Virus ◽  
Ebv Infection ◽  
Non Hodgkin Lymphoma ◽  
Acquired Immunodeficiency ◽  
Epstein Barr ◽  
Immunodeficiency Syndrome

Abstract The Epstein-Barr virus (EBV) is associated with distinct forms of human lymphoid malignancies, including the endemic (eBL) and sporadic forms of Burkitt's lymphoma (sBL) and acquired immunodeficiency syndrome- associated non-Hodgkin lymphoma (AIDS-NHL). However, whether EBV has a pathogenetic role in these tumors or is a passenger virus has not been conclusively demonstrated. One element to distinguish between these two possibilities is to determine whether EBV infection has preceded and, thus, possibly contributed to clonal expansion, or whether infection has occurred after clonal expansion and thus is unlikely to contribute to pathogenesis. Toward this end we analyzed the structure of the heterogeneous genomic termini of EBV as markers of clonal infection in a panel of eBL (11 cases), sBL (9 cases), and AIDS-NHL (10 cases) biopsies. We show that EBV termini are uniformly clonal in sBL, eBL, and AIDS-NHL, strongly suggesting that EBV infection has preceded and, thus, most likely contributed to clonal expansion in these malignancies.

Dermal Epstein Barr Virus–Associated Leiomyosarcoma: Tocsin of Acquired Immunodeficiency Syndrome in Two Children

2011 ◽  
Vol 33 (4) ◽  
pp. 392-396 ◽  
Author(s):  
Pratistadevi K Ramdial ◽  
Yetish Sing ◽  
Julian Deonarain ◽  
G P Hadley ◽  
Bhugwan Singh
Keyword(s):  
Acquired Immunodeficiency Syndrome ◽  
Epstein Barr Virus ◽  
Barr Virus ◽  
Acquired Immunodeficiency ◽  
Epstein Barr ◽  
Immunodeficiency Syndrome

Proliferation and Apoptosis-Related Gene Expression in Experimental Acquired Immunodeficiency Syndrome-Related Simian Lymphoma

Blood ◽  
1999 ◽  
Vol 93 (4) ◽  
pp. 1364-1371
Author(s):  
Esmeralda Castaños-Vélez ◽  
Thomas Heiden ◽  
Marianne Ekman ◽  
Joseph Lawrence ◽  
Gunnel Biberfeld ◽  
...  
Keyword(s):  
Gene Expression ◽  
Acquired Immunodeficiency Syndrome ◽  
Proliferative Activity ◽  
Epstein Barr Virus ◽  
Related Gene ◽  
Barr Virus ◽  
Acquired Immunodeficiency ◽  
Epstein Barr ◽  
Immunodeficiency Syndrome ◽  
Apoptosis Related Gene

Lymphomas in 10 cynomolgus monkeys infected with a simian immunodeficiency virus (SIVsm) were studied with regard to proliferative activity and apoptosis-related gene expression. All were diffuse large-cell lymphomas, showed mono or oligoclonality and a 9/10 diploid cellular DNA content. Expression of a simian homologue to Epstein-Barr virus (HVMF-1) was shown in nine cases. The lymphomas showed moderate to high proliferative activity by Ki67 immunostaining and DNA flow cytometry, and a low number of apoptotic cells detected by TdT-mediated dUTP nick-end labeling (TUNEL). Immunohistochemistry showed abundant tumor infiltrating TIA-1+ cytotoxic lymphocytes (CTL) and macrophages. Bcl-2, Mcl-1, and also Bax and Bak, but not p53 were demonstrable in the tumor cells by immunostaining. Our findings suggest a causal relationship between HVMF-1 infection and a low apoptotic index of the lymphomas due to the expression of Bcl-2. The apparent inefficient function of tumor-infiltrating CTL could be due to inactivation of CTL and/or resistance of the lymphoma cells to CTL effects. The tumors showed immunoreactivity for CD18, CD29, and CD49d, but not for CD11a, mimicking the phenotype of human Epstein-Barr virus (EBV)–related lymphomas. In summary, our observations indicate a high similarity between this simian model of acquired immunodeficiency syndrome (AIDS)-related lymphomas (ARL) and human ARL and other immunosuppression-related lymphomas.

scholarly journals Epstein-Barr virus infection precedes clonal expansion in Burkitt's and acquired immunodeficiency syndrome-associated lymphoma [see comments]

Blood ◽  
1991 ◽  
Vol 77 (5) ◽  
pp. 1092-1095 ◽  
Author(s):  
A Neri ◽  
F Barriga ◽  
G Inghirami ◽  
DM Knowles ◽  
J Neequaye ◽  
...  
Keyword(s):  
Acquired Immunodeficiency Syndrome ◽  
Epstein Barr Virus ◽  
Clonal Expansion ◽  
Epstein Barr Virus Infection ◽  
Barr Virus ◽  
Ebv Infection ◽  
Non Hodgkin Lymphoma ◽  
Acquired Immunodeficiency ◽  
Epstein Barr ◽  
Immunodeficiency Syndrome

The Epstein-Barr virus (EBV) is associated with distinct forms of human lymphoid malignancies, including the endemic (eBL) and sporadic forms of Burkitt's lymphoma (sBL) and acquired immunodeficiency syndrome- associated non-Hodgkin lymphoma (AIDS-NHL). However, whether EBV has a pathogenetic role in these tumors or is a passenger virus has not been conclusively demonstrated. One element to distinguish between these two possibilities is to determine whether EBV infection has preceded and, thus, possibly contributed to clonal expansion, or whether infection has occurred after clonal expansion and thus is unlikely to contribute to pathogenesis. Toward this end we analyzed the structure of the heterogeneous genomic termini of EBV as markers of clonal infection in a panel of eBL (11 cases), sBL (9 cases), and AIDS-NHL (10 cases) biopsies. We show that EBV termini are uniformly clonal in sBL, eBL, and AIDS-NHL, strongly suggesting that EBV infection has preceded and, thus, most likely contributed to clonal expansion in these malignancies.

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