The Role of Viral Proteins in Epstein-Barr Virus Induced Disease: Difference between revisions
No edit summary |
|||
| Line 1: | Line 1: | ||
==Introduction== | ==Introduction== | ||
<br> | <br> | ||
The Epstein-Barr Virus (EBV) is a common human herpes virus that can cause both infectious mononucleosis and lymphoproliferative disease. EBV is unique in that it infects about 95% of the adult population between 35-40 years old in the U.S. [1]. EBV is associated with cancers such as Burkitt’s Lymphoma and nasopharyngeal carcinoma [1,2]. The virus is capable of infection of host B-cells which primarily occurs via a non-lytic mechanism [2]. During this latent process, virus-derived nuclear proteins (EBNAs) and membrane proteins (LMPs) are expressed by infected host cells [2]. An advancing area of research is aimed at understanding how | The Epstein-Barr Virus (EBV) is a common human herpes virus that can cause both infectious mononucleosis and lymphoproliferative disease. EBV is unique in that it infects about 95% of the adult population between 35-40 years old in the U.S. [1]. EBV is associated with cancers such as Burkitt’s Lymphoma and nasopharyngeal carcinoma [1,2]. The virus is capable of infection of host B-cells which primarily occurs via a non-lytic mechanism [2]. During this latent process, virus-derived nuclear proteins (EBNAs) and membrane proteins (LMPs) are expressed by infected host cells [2]. An advancing area of research is aimed at understanding how viral proteins may play a role in lymphoproliferative disease. LMP-1 is one of these viral membranous proteins that may induce indefinite, tumorigenic, replication in infected B-cells [3]. While EBV infections usually only cause mild symptoms, attempts to develop treatments and antivirals have generally been unsuccessful [1]. The the prevalence of chronic infections that may reactivate make it particularly hard to contain spread between hosts [1]. Due to EBV's putative role in carcinogenesis and the limited success in development of antivirals to combat infection, it is essential to develop a deeper understanding of the mechanisms by which the virus alters host cells. | ||
==References== | ==References== | ||
Revision as of 16:56, 13 November 2012
Introduction
The Epstein-Barr Virus (EBV) is a common human herpes virus that can cause both infectious mononucleosis and lymphoproliferative disease. EBV is unique in that it infects about 95% of the adult population between 35-40 years old in the U.S. [1]. EBV is associated with cancers such as Burkitt’s Lymphoma and nasopharyngeal carcinoma [1,2]. The virus is capable of infection of host B-cells which primarily occurs via a non-lytic mechanism [2]. During this latent process, virus-derived nuclear proteins (EBNAs) and membrane proteins (LMPs) are expressed by infected host cells [2]. An advancing area of research is aimed at understanding how viral proteins may play a role in lymphoproliferative disease. LMP-1 is one of these viral membranous proteins that may induce indefinite, tumorigenic, replication in infected B-cells [3]. While EBV infections usually only cause mild symptoms, attempts to develop treatments and antivirals have generally been unsuccessful [1]. The the prevalence of chronic infections that may reactivate make it particularly hard to contain spread between hosts [1]. Due to EBV's putative role in carcinogenesis and the limited success in development of antivirals to combat infection, it is essential to develop a deeper understanding of the mechanisms by which the virus alters host cells.
References
[1]"Epstein-Barr Virus and Infectious Mononucleosis." Centers for Disease Control. http://www.cdc.gov/ncidod/diseases/ebv.htm. Accessed: 11/3/12.
[2]
