Kaposi's sarcoma pathophysiology
|
Kaposi's sarcoma Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Kaposi's sarcoma pathophysiology On the Web |
|
American Roentgen Ray Society Images of Kaposi's sarcoma pathophysiology |
|
Risk calculators and risk factors for Kaposi's sarcoma pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Haytham Allaham, M.D. [2]
Overview
Pathogenesis
- Kaposi's sarcoma arises from endothelial cells, which are epithelial cells that normally lines the interior surface of blood vessels and lymphatic vessels.
- Kaposi's sarcoma is mainly caused by an infection with Human herpes virus 8 (HHV8), which is also known as Kaposi's sarcoma-associated herpes virus (KSHV).
- HHV8 is usually transmitted through saliva via close sexual contact.
- Another minor route of transmission for HHV8 is through organ transplantation.
- The oncogenesis of HHV8 infection, which results in the development of Kaposi's sarcoma, is due to a number of human cellular genes that have been incorporated through molecular piracy into the viral DNA sequence.
- The genes acquired by HHV8 will augment the cellular proliferation pathways of infected cells through various mediators and DNA synthesis proteins such as:
- Complement-binding protein
- IL-6
- BCL-2
- Cyclin-D
- Interferon regulatory factor
- Flice inhibitory protein (FLIP)
- Dihydrofolate reductase
- Thymidine kinase
- Thymidylate synthetase
- DNA polymerase
- The augmentation of cellular pathways will protect the virus from the immune system attacks and allow a continuous viral replication during the latency period.