Epstein-Barr virus (EBV) and EBV-associated lymphomas: Difference between revisions
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==Identifying Latency Patterns of EBV Infection== | ==Identifying Latency Patterns of EBV Infection== | ||
During primary in vivo infection, EBV preferentially infects B-lymphocytes by binding to the CD21 receptor on the cell surface, it will also bind to HLA class II molecules as a co-receptor. In most of the patients, the EBV episome would remain in the latent cycle in resting memory B cells after the primary infection while developing strategies to alter the pattern of the host’s cytotoxic T-lymphocyte (CTL) gene expression. Although there are nearly 100 viral proteins in a regular EBV genome, after infection, the infected resting memory B cells will limit the gene expression to nine viral latent proteins to evade immune recognition. The nine viral latent proteins are composed of six nuclear antigens EBNAs-1, -2, -3a, -3b, -3c, and -LP as well as three latent membrane proteins LMP-1, -2a, -2b. 2 small non-coding RNAs, EBER-1, EBER-2, and BamHI-A rightward transcripts (BART) are also expressed. The expression of nuclear antigens maintains the viral genome, they are also responsible for controlling the expression patterns of the three latent membrane proteins. Different expression combinations of EBNAs and LMPs can lead to different EBV latency programs and the associated lymphomas <ref | During primary in vivo infection, EBV preferentially infects B-lymphocytes by binding to the CD21 receptor on the cell surface, it will also bind to HLA class II molecules as a co-receptor. In most of the patients, the EBV episome would remain in the latent cycle in resting memory B cells after the primary infection while developing strategies to alter the pattern of the host’s cytotoxic T-lymphocyte (CTL) gene expression. Although there are nearly 100 viral proteins in a regular EBV genome, after infection, the infected resting memory B cells will limit the gene expression to nine viral latent proteins to evade immune recognition. The nine viral latent proteins are composed of six nuclear antigens EBNAs-1, -2, -3a, -3b, -3c, and -LP as well as three latent membrane proteins LMP-1, -2a, -2b. 2 small non-coding RNAs, EBER-1, EBER-2, and BamHI-A rightward transcripts (BART) are also expressed. The expression of nuclear antigens maintains the viral genome, they are also responsible for controlling the expression patterns of the three latent membrane proteins. Different expression combinations of EBNAs and LMPs can lead to different EBV latency programs and the associated lymphomas <ref>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3305910/</ref>. | ||
Type I latency is only seen in Burkitt’s lymphoma (BL) and selectively express EBNA-1. Type II latency expresses EBNA-1 along with LMP-1 and LMP-2, the common lymphoma for type II latency to be found are Hodgkin’s lymphoma (HL) and peripheral T-cell lymphoma (PTCL). The third and last EBV latency program type III, is commonly found in PTLD and AIDS-related lymphoma. All nine EBV latent proteins are expressed in type III latency | Type I latency is only seen in Burkitt’s lymphoma (BL) and selectively express EBNA-1. Type II latency expresses EBNA-1 along with LMP-1 and LMP-2, the common lymphoma for type II latency to be found are Hodgkin’s lymphoma (HL) and peripheral T-cell lymphoma (PTCL). The third and last EBV latency program type III, is commonly found in PTLD and AIDS-related lymphoma. All nine EBV latent proteins are expressed in type III latency. | ||
==Section 2== | ==Section 2== | ||
Revision as of 07:16, 7 April 2021
By Yangyang Liu (Kenyon '23)
Introduction
Epstein-Barr virus (EBV), formally called Human gammaherpesvirus 4, are a group within the Lymphocryptovirus genus of the Herpesviridae family. EBVise double-stranded DNA viruses that use RNA polymerase for mRNA synthesis based on their negative-strand as the template. EBV Infection occurs through oral transfer of saliva as well as genital secretions and more than 90% of normal adults would gain adaptive immunity after their primary EBV infection. The remaining EBV virus would remain in an asymptomatic latent state for a lifetime within resting B-cells, and a healthy adult with a working immune system would be able to contain the infection with the help of their cytotoxic T cells (CTLs), lymphocyte CD8+ and CD4+, and natural killer (NK) cells [1]. Only a small subset encountering life-threatening diseases due to them unable in maintaining the virus within the latent state. In an uncontrolled situation, EBV-driven lymphoproliferative disorders and lymphomas could develop with the patients. EBV-associated cancers are a common example among the ~15% of all human cancers involving a virus infection [2].
Some of the most well-known illnesses that are caused by EBV are mononucleosis, Burkitt’s lymphoma, Hodgkin’s lymphoma, non-Hodgkin lymphoma, post-transplant lymphoproliferative disease (PTLD), nasopharyngeal carcinoma, and numerous other types of cancer [3]. So far, there is limited success in antivirals development to combat EBV infection. With EBV’s putative role in carcinogenesis, it is important to learn about the mechanisms by which the virus alters host cell characteristics and thus evades the immune system of the hosts. This page investigates how different latency patterns of EBV infection could lead to numerous types of lymphoma, the role of EBV in rare EBV-associated NK-cell lymphoproliferative diseases, as well as possible treatment for EBV-T/NK-LPDs.
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Type I latency is only seen in Burkitt’s lymphoma (BL) and selectively express EBNA-1. Type II latency expresses EBNA-1 along with LMP-1 and LMP-2, the common lymphoma for type II latency to be found are Hodgkin’s lymphoma (HL) and peripheral T-cell lymphoma (PTCL). The third and last EBV latency program type III, is commonly found in PTLD and AIDS-related lymphoma. All nine EBV latent proteins are expressed in type III latency.
Section 2
Section 3
Section 4
Conclusion
See Also
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Stomach
Small Intestine
The Hologenome Theory of Evolution
Microbes and Animal Behavior
Intestinal Microflora and Antibiotic Resistance
References
- ↑ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3305910/#:~:text=Epstein%2DBarr%20virus%20(EBV),driven%20lymphoproliferative%20disorders%20and%20lymphomas
- ↑ https://onlinelibrary.wiley.com/doi/abs/10.1002/rmv.456
- ↑ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3415781/
- ↑ Hodgkin, J. and Partridge, F.A. "Caenorhabditis elegans meets microsporidia: the nematode killers from Paris." 2008. PLoS Biology 6:2634-2637.
- ↑ Bartlett et al.: Oncolytic viruses as therapeutic cancer vaccines. Molecular Cancer 2013 12:103.
Authored for BIOL 238 Microbiology, taught by Joan Slonczewski, 2021, Kenyon College.
