The Role of Viral Proteins in Epstein-Barr Virus Induced Disease: Difference between revisions

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==Introduction==
==Introduction==


[[Image:bcd28_koala-retrovirus.jpg|thumb|800px|right|<i>Phascolarctos cinereus</i>, the lone host of the Koala retrovirus.  [http://go-off-grid.com/solar-power/wind-power-news/koalas-threatened-with-aids-like-epidemic-extinction-looms].]]
[[Image:EBV1.jpg|thumb|400px|right|The original electron micrographs of cultured Burkits Lymphoma tissue published by Epstein and Barr in 1964. V denotes the presence of EBV virions.  [http://ac.els-cdn.com/S0140673664915247/1-s2.0-S0140673664915247-main.pdf?_tid=c1822c94-2dc6-11e2-9201-00000aab0f27&acdnat=1352834424_53e11ef091d573d29573b32f40b44001].]]


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, and primarily proliferates 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]. In a sense, the LMP-1 acts to "transform" these B-cells into an immortalized, proliferating line. While EBV infections usually only cause mild symptoms, attempts to develop treatments and antivirals have generally been unsuccessful [1]. It is particularly difficult to control spread between hosts as chronic infections may reactivate, allowing symptom-free carriers to continue to transmit the virus years after initial infection [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.
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, and primarily proliferates 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]. In a sense, the LMP-1 acts to "transform" these B-cells into an immortalized, proliferating line. While EBV infections usually only cause mild symptoms, attempts to develop treatments and antivirals have generally been unsuccessful [1]. It is particularly difficult to control spread between hosts as chronic infections may reactivate, allowing symptom-free carriers to continue to transmit the virus years after initial infection [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.

Revision as of 19:26, 13 November 2012

Introduction

The original electron micrographs of cultured Burkits Lymphoma tissue published by Epstein and Barr in 1964. V denotes the presence of EBV virions. [1].

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, and primarily proliferates 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]. In a sense, the LMP-1 acts to "transform" these B-cells into an immortalized, proliferating line. While EBV infections usually only cause mild symptoms, attempts to develop treatments and antivirals have generally been unsuccessful [1]. It is particularly difficult to control spread between hosts as chronic infections may reactivate, allowing symptom-free carriers to continue to transmit the virus years after initial infection [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.

Virus Classification and Discovery

Baltimore Classification: Group 1 (ds DNA genome)

Family: Herpesviridae

Subfamily: Gammaherpesvirinae

Genus: Lymphocryptovirus

Species: Human Herpes Virus 4 (HHV-4)

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] Young LS,Rickinson AB. 2004. Epstein-Barr Virus: 40 Years On. Nature Reviews. 4:757-768.

[3]