Imperial College London
Alternate

ProfessorPaiviOjala

Faculty of Medicine, Department of Infectious Disease

Visiting Professor
 
 
 
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Contact

 

+44 (0)20 7594 3971p.ojala Website

 
 
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Location

 

443Medical SchoolSt Mary's Campus

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Summary

 

Publications

Citation

BibTex format

@article{Gramolelli:2017:10.1016/j.coviro.2017.09.002,
author = {Gramolelli, S and Ojala, PM},
doi = {10.1016/j.coviro.2017.09.002},
journal = {CURRENT OPINION IN VIROLOGY},
pages = {156--162},
title = {Kaposi's sarcoma herpesvirus-induced endothelial cell reprogramming supports viral persistence and contributes to Kaposi's sarcoma tumorigenesis},
url = {http://dx.doi.org/10.1016/j.coviro.2017.09.002},
volume = {26},
year = {2017}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - 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.
AU  - Gramolelli,S
AU  - Ojala,PM
DO  - 10.1016/j.coviro.2017.09.002
EP  - 162
PY  - 2017///
SN  - 1879-6257
SP  - 156
TI  - Kaposi's sarcoma herpesvirus-induced endothelial cell reprogramming supports viral persistence and contributes to Kaposi's sarcoma tumorigenesis
T2  - CURRENT OPINION IN VIROLOGY
UR  - http://dx.doi.org/10.1016/j.coviro.2017.09.002
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000415782500025&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - http://hdl.handle.net/10044/1/59369
VL  - 26
ER  -
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