Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2018 Jun 13:8:211.
doi: 10.3389/fonc.2018.00211. eCollection 2018.

Epstein-Barr Virus Epidemiology, Serology, and Genetic Variability of LMP-1 Oncogene Among Healthy Population: An Update

Maria K Smatti  1 , Duaa W Al-Sadeq  2 , Nadima H Ali  1 , Gianfranco Pintus  2 , Haissam Abou-Saleh  3 , Gheyath K Nasrallah  1   2
Affiliations
Review

Epstein-Barr Virus Epidemiology, Serology, and Genetic Variability of LMP-1 Oncogene Among Healthy Population: An Update

Maria K Smatti et al. Front Oncol. .

Abstract

The Epstein-Barr virus (EBV) is a DNA lymphotropic herpesvirus and the causative agent of infectious mononucleosis. EBV is highly prevalent since it affects more than 90% of individuals worldwide and has been linked to several malignancies including PTLDs, which are one of the most common malignancies following transplantation. Among all the EBV genes, most of the recent investigations focused on studying the LMP-1 oncogene because of its high degree of polymorphism and association with tumorigenic activity. There are two main EBV genotypes, Type 1 and 2, distinguished by the differences in the EBNA-2 gene. Further sub genotyping can be characterized by analyzing the LMP-1 gene variation. The virus primarily transmits through oral secretions and persists as a latent infection in human B-cells. However, it can be transmitted through organ transplantations and blood transfusions. In addition, symptoms of EBV infection are not distinguishable from other viral infections, and therefore, it remains questionable whether there is a need to screen for EBV prior to blood transfusion. Although the process of leukoreduction decreases the viral copies present in the leukocytes, it does not eliminate the risk of EBV transmission through blood products. Here, we provide a review of the EBV epidemiology and the genetic variability of the oncogene LMP-1. Then, we underscore the findings of recent EBV seroprevalence and viremia studies among blood donors as a highly prevalent transfusion transmissible oncovirus.

Keywords: Epstein–Barr virus; LMP-1 oncogene; blood donors; seroprevalence; transfusion; viremia.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Schematic representation describing the mechanism by which LMP-1 protein affects cell signal transduction. CTAR1 and CTAR2 bind to TRAF proteins and activate NF-κB and JNK–AP-1 pathways. LMP-1 can block cell apoptosis signals by activating BCL2A1.
Figure 2
Figure 2
Epstein–Barr virus (EBV) life cycle in healthy carriers. The infection begins when EBV infect epithelial cells and naïve B cells of the oral cavity. EBV genome will be transported to the nucleus of B cell where it will replicate and results in the proliferation of B cells. Latency occurs when EBV downregulate most of its protein-encoding genes. Later, as cells recirculate between peripheral and oral compartments, resting B cells will be reactivated and cause viral shedding.
Figure 3
Figure 3
A scheme of serological response to Epstein–Barr virus (EBV) infection. Viral capsid antigens (VCA)-IgM is detected in the active phase of infection and then declines in convalescence. VCA-IgG increases at the same time of VCA-IgM, but it remains positive for life indicating past infection. Epstein Barr nuclear antigens (EBNA) antibodies are detectable late in the phase of infection and also remain positive. Early antigens (EA) antibodies to the class R or D increase in the acute phase of infection and decline after convalescence.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. CDC. Epstein-Barr Virus and Infectious Mononucleosis. (2016). Available from: https://www.cdc.gov/epstein-barr/about-mono.html.
    1. Epstein MA, Achong BG, Barr YM. Virus particles in cultured lymphoblasts from Burkitt’s lymphoma. Lancet (1964) 1(7335):702–3.10.1016/S0140-6736(64)91524-7 - DOI - PubMed
    1. Young LS, Rickinson AB. Epstein-Barr virus: 40 years on. Nat Rev Cancer (2004) 4(10):757–68.10.1038/nrc1452 - DOI - PubMed
    1. Tzellos S, Farrell PJ. Epstein-Barr virus sequence variation-biology and disease. Pathogens (2012) 1(2):156–74.10.3390/pathogens1020156 - DOI - PMC - PubMed
    1. Santpere G, Darre F, Blanco S, Alcami A, Villoslada P, Mar Albà M, et al. Genome-wide analysis of wild-type Epstein-Barr virus genomes derived from healthy individuals of the 1,000 genomes project. Genome Biol Evol (2014) 6(4):846–60.10.1093/gbe/evu054 - DOI - PMC - PubMed

LinkOut - more resources