Kaposi's sarcoma herpesvirus-induced endothelial cell reprogramming supports viral persistence and contributes to Kaposi's sarcoma tumorigenesis

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http://hdl.handle.net/10138/232265

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Gramolelli , S & Ojala , P M 2017 , ' Kaposi's sarcoma herpesvirus-induced endothelial cell reprogramming supports viral persistence and contributes to Kaposi's sarcoma tumorigenesis ' Current opinion in virology , vol 26 , pp. 156-162 . DOI: 10.1016/j.coviro.2017.09.002

Title: Kaposi's sarcoma herpesvirus-induced endothelial cell reprogramming supports viral persistence and contributes to Kaposi's sarcoma tumorigenesis
Author: Gramolelli, Silvia; Ojala, Päivi M.
Contributor: University of Helsinki, Research Programs Unit
University of Helsinki, Research Programs Unit
Belongs to series: Current opinion in virology
ISSN: 1879-6257
Abstract: Kaposi's sarcoma (KS) is an endothelial tumor causally linked to Kaposi's sarcoma herpesvirus (KSHV) infection. At early stages of KS, inflammation and aberrant neoangiogenesis are predominant, while at late stages the disease is characterized by the proliferation of KSHV-infected spindle cells (SC). Since KSHV infection modifies the endothelial cell (EC) identity, the origin of SCs remains elusive. Yet, pieces of evidence indicate the lymphatic origin. KSHV-infected ECs display increased proliferative, angiogenic and migratory capacities which account for KS oncogenesis. Here we propose a model in which KSHV reprograms the EC identity, induces DNA damage and establishes a dysregulated gene expression program involving interplay of latent and lytic genes allowing continuous. reinfection of ECs attracted to the tumor by the secretion of virus-induced cellular factors.
URI: http://hdl.handle.net/10138/232265
Date: 2017-10
Subject: MULTICENTRIC CASTLEMANS-DISEASE
TO-MESENCHYMAL TRANSITION
CAVITY-BASED LYMPHOMAS
DNA-DAMAGE RESPONSE
HUMAN TUMOR-VIRUSES
SPINDLE CELLS
GENE-EXPRESSION
IN-VITRO
LYTIC REPLICATION
LYMPHATIC-SYSTEM
3111 Biomedicine
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