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Updated: May 12, 2026

Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus (KSHV)
Published on: September 15, 2010
Kaposi's sarcoma and its associated herpesvirus
Enrique A Mesri1, Ethel Cesarman, Chris Boshoff
1Viral Oncology Program, Developmental Center for AIDS Research, and Department of Microbiology & Immunology, Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, 1,550 NW 10th Avenue, 109 Papanicolau Building, Miami, Florida 33136, USA. emesri@med.miami.edu
Kaposi's sarcoma (KS), a cancer common in untreated HIV patients, is caused by Kaposi's sarcoma-associated herpesvirus (KSHV). This review details how KSHV's latent and lytic proteins drive KS development through cell proliferation and inflammation.
Area of Science:
- Oncology
- Virology
- Immunology
Background:
- Kaposi's sarcoma (KS) is the most frequent cancer in individuals with untreated HIV infection.
- Kaposi's sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8 (HHV8), is the infectious agent responsible for KS.
- Understanding KSHV's role is crucial for managing this opportunistic infection.
Purpose of the Study:
- To review the epidemiology of KS and KSHV.
- To elucidate the mechanisms by which KSHV induces KS.
- To summarize recent advancements in understanding KSHV-driven oncogenesis.
Main Methods:
- Literature review of studies on KS and KSHV epidemiology and mechanisms.
- Analysis of KSHV gene products involved in KS pathogenesis.
- Synthesis of current knowledge on viral oncogenesis.
Main Results:
- KSHV latent transcripts (e.g., LANA, viral cyclin, viral FLIP, microRNAs) promote cell proliferation and inhibit apoptosis.
- KSHV lytic proteins (e.g., viral G protein-coupled receptor, K1, viral IL-6, viral chemokines) contribute to KS lesions via paracrine neoplasia.
- These viral factors collectively drive the angioproliferative and inflammatory characteristics of KS.
Conclusions:
- KSHV employs a multi-faceted strategy involving both latent and lytic gene products to induce KS.
- The interplay of viral proteins disrupts normal cellular processes, leading to tumor formation.
- Further research into these mechanisms can inform therapeutic strategies against KS.
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