Kaposi's sarcoma pathophysiology: Difference between revisions
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* 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 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). | * 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 | * HHV8 is usually transmitted through saliva via close sexual contact. | ||
* Another minor route of transmission for HHV8 is through organ transplantation. | * 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. | |||
==Genetics== | ==Genetics== | ||
==Associated Conditions== | ==Associated Conditions== | ||
Revision as of 13:14, 19 January 2016
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Kaposi's sarcoma Microchapters |
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Kaposi's sarcoma pathophysiology On the Web |
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American Roentgen Ray Society Images of Kaposi's sarcoma pathophysiology |
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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.