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[Human herpes virus 8: molecules determinants of oncogenesis and modulation of the immune response].

Authors: E, Boulanger; A, Gessain;

[Human herpes virus 8: molecules determinants of oncogenesis and modulation of the immune response].

Abstract

Human herpesvirus 8 (HHV8), also called Kaposi sarcoma-associated herpesvirus (KSHV), is a human c2-herpesvirus, characterized by B lymphotropism and oncogenic properties. HHV8 is the etiological agent of Kaposi sarcoma, and of rare B cell lymphoproliferative disorders mostly observed in immunocompromised hosts (patients with AIDS, transplant organ recipients) such as primary effusion lymphoma and the plasma cell variant of multicentric Castleman disease. HHV8 contains numerous open reading frames encoding homologs to cellular genes involved in cell growth and apoptosis control. Among these are signal-transducing transmembrane proteins, secreted cytokine and chemokine homologs, transcriptional modulators, cell cycle regulators and apoptosis inhibitors. Several immune modulation strategies are used by HHV8 to target both innate and adaptative immunity, including complement activity control, Th2 chemotaxis, inhibition of type I and II interferons and B cell receptor signalling, and downregulation of class I histocompatibility antigens.

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
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