↓ Skip to main content

Epigenetic Contributions in Autoimmune Disease

Overview of attention for book
Attention for Chapter 7: Epigenetic dysregulation of epstein-barr virus latency and development of autoimmune disease.
Altmetric Badge

Mentioned by

facebook
2 Facebook pages

Citations

dimensions_citation
4 Dimensions

Readers on

mendeley
34 Mendeley
You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output. Click here to find out more.
Chapter title
Epigenetic dysregulation of epstein-barr virus latency and development of autoimmune disease.
Chapter number 7
Book title
Epigenetic Contributions in Autoimmune Disease
Published in
Advances in experimental medicine and biology, January 2011
DOI 10.1007/978-1-4419-8216-2_7
Pubmed ID
Book ISBNs
978-1-4419-8215-5, 978-1-4419-8216-2
Authors

Hans Helmut Niller, Hans Wolf, Eva Ay, Janos Minarovits, Niller, Hans Helmut, Wolf, Hans, Ay, Eva, Minarovits, Janos

Abstract

Epstein-Barr virus (EBV) is ahumanherpesvirus thatpersists in the memory B-cells of the majority of the world population in a latent form. Primary EBV infection is asymptomatic or causes a self-limiting disease, infectious mononucleosis. Virus latency is associated with a wide variety of neoplasms whereof some occur in immune suppressed individuals. Virus production does not occur in strict latency. The expression of latent viral oncoproteins and nontranslated RNAs is under epigenetic control via DNA methylation and histone modifications that results either in a complete silencing of the EBV genome in memory B cells, or in a cell-type dependent usage of a couple of latency promoters in tumor cells, germinal center B cells and lymphoblastoid cells (LCL, transformed by EBV in vitro). Both, latent and lytic EBV proteins elicit a strong immune response. In immune suppressed and infectious mononucleosis patients, an increased viral load can be detected in the blood. Enhanced lytic replication may result in new infection- and transformation-events and thus is a risk factor both for malignant transformation and the development of autoimmune diseases. An increased viral load or a changed presentation of a subset of lytic or latent EBV proteins that cross-react with cellular antigens may trigger pathogenic processes through molecular mimicry that result in multiple sclerosis (MS), systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 34 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 1 3%
Unknown 33 97%

Demographic breakdown

Readers by professional status Count As %
Researcher 7 21%
Student > Bachelor 6 18%
Other 3 9%
Professor > Associate Professor 2 6%
Student > Ph. D. Student 2 6%
Other 3 9%
Unknown 11 32%
Readers by discipline Count As %
Medicine and Dentistry 9 26%
Biochemistry, Genetics and Molecular Biology 3 9%
Immunology and Microbiology 3 9%
Neuroscience 2 6%
Pharmacology, Toxicology and Pharmaceutical Science 1 3%
Other 3 9%
Unknown 13 38%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 30 December 2015.
All research outputs
#20,278,934
of 24,931,592 outputs
Outputs from Advances in experimental medicine and biology
#3,598
of 5,247 outputs
Outputs of similar age
#172,253
of 192,672 outputs
Outputs of similar age from Advances in experimental medicine and biology
#27
of 46 outputs
Altmetric has tracked 24,931,592 research outputs across all sources so far. This one is in the 10th percentile – i.e., 10% of other outputs scored the same or lower than it.
So far Altmetric has tracked 5,247 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.8. This one is in the 18th percentile – i.e., 18% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 192,672 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 5th percentile – i.e., 5% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 46 others from the same source and published within six weeks on either side of this one. This one is in the 10th percentile – i.e., 10% of its contemporaries scored the same or lower than it.