The Role of Viral Proteins in Epstein-Barr Virus Induced Disease

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, 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.

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]