Familial clustering of classic Kaposi sarcoma

Emma Guttman-Yassky; Adina Cohen; Zippi Kra-Oz; Rachel Friedman-Birnbaum; Elli Sprecher; Neli Zaltzman; Eitan Friedman; Michael Silbermann; Dina Rubin; Shai Linn; Dennis Whitby; Osnat Gideoni; Shimon Pollack; Reuven Bergman; Ronit Sarid

doi:10.1086/386308

Familial clustering of classic Kaposi sarcoma

Emma Guttman-Yassky, Adina Cohen, Zippi Kra-Oz, Rachel Friedman-Birnbaum, Elli Sprecher, Neli Zaltzman, Eitan Friedman, Michael Silbermann, Dina Rubin, Shai Linn, Dennis Whitby, Osnat Gideoni, Shimon Pollack, Reuven Bergman, Ronit Sarid

The Mina and Everard Goodman Faculty of Life Sciences

Research output: Contribution to journal › Article › peer-review

38 Scopus citations

Abstract

It is widely accepted that there is a causal association between Kaposi sarcoma-associated herpesvirus (KSHV) and Kaposi sarcoma (KS). However, the majority of individuals infected with KSHV never develop KS. Here, we present a unique familial case of classic KS, in which the disease occurs in 4 siblings who have no recognized underlying immunodeficiency. We examine risk factors that could play a role in this condition, including KSHV infection, KSHV DNA load, genetic variants of KSHV, infection with additional viruses, interleukin-6-promoter polymorphism, and HLA genotype. We hypothesize that a genetic susceptibility to KS, in combination with KSHV infection, may play an important role in the presented familial case.

Original language	English
Pages (from-to)	2023-2026
Number of pages	4
Journal	Journal of Infectious Diseases
Volume	189
Issue number	11
DOIs	https://doi.org/10.1086/386308
State	Published - 1 Jun 2004

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10.1086/386308

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title = "Familial clustering of classic Kaposi sarcoma",

abstract = "It is widely accepted that there is a causal association between Kaposi sarcoma-associated herpesvirus (KSHV) and Kaposi sarcoma (KS). However, the majority of individuals infected with KSHV never develop KS. Here, we present a unique familial case of classic KS, in which the disease occurs in 4 siblings who have no recognized underlying immunodeficiency. We examine risk factors that could play a role in this condition, including KSHV infection, KSHV DNA load, genetic variants of KSHV, infection with additional viruses, interleukin-6-promoter polymorphism, and HLA genotype. We hypothesize that a genetic susceptibility to KS, in combination with KSHV infection, may play an important role in the presented familial case.",

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AU - Guttman-Yassky, Emma

AU - Cohen, Adina

AU - Kra-Oz, Zippi

AU - Friedman-Birnbaum, Rachel

AU - Sprecher, Elli

AU - Zaltzman, Neli

AU - Friedman, Eitan

AU - Silbermann, Michael

AU - Rubin, Dina

AU - Linn, Shai

AU - Whitby, Dennis

AU - Gideoni, Osnat

AU - Pollack, Shimon

AU - Bergman, Reuven

AU - Sarid, Ronit

PY - 2004/6/1

Y1 - 2004/6/1

N2 - It is widely accepted that there is a causal association between Kaposi sarcoma-associated herpesvirus (KSHV) and Kaposi sarcoma (KS). However, the majority of individuals infected with KSHV never develop KS. Here, we present a unique familial case of classic KS, in which the disease occurs in 4 siblings who have no recognized underlying immunodeficiency. We examine risk factors that could play a role in this condition, including KSHV infection, KSHV DNA load, genetic variants of KSHV, infection with additional viruses, interleukin-6-promoter polymorphism, and HLA genotype. We hypothesize that a genetic susceptibility to KS, in combination with KSHV infection, may play an important role in the presented familial case.

AB - It is widely accepted that there is a causal association between Kaposi sarcoma-associated herpesvirus (KSHV) and Kaposi sarcoma (KS). However, the majority of individuals infected with KSHV never develop KS. Here, we present a unique familial case of classic KS, in which the disease occurs in 4 siblings who have no recognized underlying immunodeficiency. We examine risk factors that could play a role in this condition, including KSHV infection, KSHV DNA load, genetic variants of KSHV, infection with additional viruses, interleukin-6-promoter polymorphism, and HLA genotype. We hypothesize that a genetic susceptibility to KS, in combination with KSHV infection, may play an important role in the presented familial case.

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JF - Journal of Infectious Diseases

IS - 11

ER -

Familial clustering of classic Kaposi sarcoma

Abstract

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