TY - JOUR
T1 - Kaposi's sarcoma and its associated herpesvirus
AU - Mesri, Enrique A.
AU - Cesarman, Ethel
AU - Boshoff, Chris
N1 - Funding Information:
E.A.M. is supported by US National Institutes of Health grants CA75918 and CA136387, and C.B. by Cancer Research UK, the Medical Research Council and the University College London and University College London Hopsitals Comprehensive Biomedical Research Centre.
PY - 2010/10
Y1 - 2010/10
N2 - Kaposi's sarcoma (KS) is the most common cancer in HIV-infected untreated individuals. Kaposi's sarcoma-associated herpesvirus (KSHV; also known as human herpesvirus 8 (HHV8)) is the infectious cause of this neoplasm. In this Review we describe the epidemiology of KS and KSHV, and the insights into the remarkable mechanisms through which KSHV can induce KS that have been gained in the past 16 years. KSHV latent transcripts, such as latency-associated nuclear antigen (LANA), viral cyclin, viral FLIP and viral-encoded microRNAs, drive cell proliferation and prevent apoptosis, whereas KSHV lytic proteins, such as viral G protein-coupled receptor, K1 and virally encoded cytokines (viral interleukin-6 and viral chemokines) further contribute to the unique angioproliferative and inflammatory KS lesions through a mechanism called paracrine neoplasia.
AB - Kaposi's sarcoma (KS) is the most common cancer in HIV-infected untreated individuals. Kaposi's sarcoma-associated herpesvirus (KSHV; also known as human herpesvirus 8 (HHV8)) is the infectious cause of this neoplasm. In this Review we describe the epidemiology of KS and KSHV, and the insights into the remarkable mechanisms through which KSHV can induce KS that have been gained in the past 16 years. KSHV latent transcripts, such as latency-associated nuclear antigen (LANA), viral cyclin, viral FLIP and viral-encoded microRNAs, drive cell proliferation and prevent apoptosis, whereas KSHV lytic proteins, such as viral G protein-coupled receptor, K1 and virally encoded cytokines (viral interleukin-6 and viral chemokines) further contribute to the unique angioproliferative and inflammatory KS lesions through a mechanism called paracrine neoplasia.
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U2 - 10.1038/nrc2888
DO - 10.1038/nrc2888
M3 - Review article
C2 - 20865011
AN - SCOPUS:77957121811
VL - 10
SP - 707
EP - 719
JO - Nature Reviews Cancer
JF - Nature Reviews Cancer
SN - 1474-175X
IS - 10
ER -