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See Latest ArticlesHuman herpesvirus-8 and kaposi sarcoma after kidney transplantation: Mechanisms of tumor genesis
Iranian Journal of Kidney Diseases, 08/03/09
Ahmadpoor P – Article reviews the tumor genesis mechanism of human herpesviruses (HHV)-8 in kidney transplant recipients.
- The incidence of iatrogenic Kaposi sarcoma (KS), which develops after organ transplantation, is 500 times higher than that in general population
- HHV-8 enters the cell by 2 glycoproteins called gp and gpk8.1
- Gp binds to glycosaminoglycans and integrin α3β1, and gp8.1 binds to heparan sulfate
- After entering the cell, the virus interferes with different pathways important for cell proliferation like cyclins, CDK, PI3K, and Akt pathways
- HHV-8 genome has 90 open reading frames
- HHV-8 is famous for “molecular piracy” that is the ability of the virus to produce proteins that are quite similar to human proteins but with different functions such as production of viral IL-6 or viral macrophage inflammatory ptoyeins
- By this capability, HHV-8 is able to control key aspects of cell regulation, allowing the cell to replicate, to prevent cell death, and to shut off immune responses in infected cells
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Today in Transplantation...keeping you current
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Transplant Nephrectomy Associates with Improved Survival in Patients with Failed Renal Allograft
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Today in Nephrology...keeping you current
Receive free subspecialty "5-minute updates" via email
The Role of the Mammalian Target Of Rapamycin (mTOR) in Renal Disease
Journal of the American Society of Nephrology, 11/25/09
Tracing the Origin of Glomerular Extracapillary Lesions from Parietal Epithelial Cells
Journal of the American Society of Nephrology, 11/25/09
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