Epstein-Barr Virus and Systemic Lupus Erythematosus
The etiology of SLE is not fully established. SLE is a disease with periods of waning disease activity and intermittent flares. This fits well in theory to a latent virus infection, which occasionally switches to lytic cycle, and EBV infection has for long been suspected to be involved. This paper r...
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Hindawi Publishing Corporation
2012
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3395176/ |
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pubmed-33951762012-07-18 Epstein-Barr Virus and Systemic Lupus Erythematosus Draborg, Anette Holck Duus, Karen Houen, Gunnar Review Article The etiology of SLE is not fully established. SLE is a disease with periods of waning disease activity and intermittent flares. This fits well in theory to a latent virus infection, which occasionally switches to lytic cycle, and EBV infection has for long been suspected to be involved. This paper reviews EBV immunobiology and how this is related to SLE pathogenesis by illustrating uncontrolled reactivation of EBV as a disease mechanism for SLE. Studies on EBV in SLE patients show enlarged viral load, abnormal expression of viral lytic genes, impaired EBV-specific T-cell response, and increased levels of EBV-directed antibodies. These results suggest a role for reactivation of EBV infection in SLE. The increased level of EBV antibodies especially comprises an elevated titre of IgA antibodies, and the total number of EBV-reacting antibody isotypes is also enlarged. As EBV is known to be controlled by cell-mediated immunity, the reduced EBV-specific T-cell response in SLE patients may result in defective control of EBV causing frequent reactivation and expression of lytic cycle antigens. This gives rise to enhanced apoptosis and amplified cellular waste load resulting in activation of an immune response and development of EBV-directed antibodies and autoantibodies to cellular antigens. Hindawi Publishing Corporation 2012 2012-07-03 /pmc/articles/PMC3395176/ /pubmed/22811739 http://dx.doi.org/10.1155/2012/370516 Text en Copyright © 2012 Anette Holck Draborg et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Draborg, Anette Holck Duus, Karen Houen, Gunnar |
| spellingShingle |
Draborg, Anette Holck Duus, Karen Houen, Gunnar Epstein-Barr Virus and Systemic Lupus Erythematosus |
| author_facet |
Draborg, Anette Holck Duus, Karen Houen, Gunnar |
| author_sort |
Draborg, Anette Holck |
| title |
Epstein-Barr Virus and Systemic Lupus Erythematosus |
| title_short |
Epstein-Barr Virus and Systemic Lupus Erythematosus |
| title_full |
Epstein-Barr Virus and Systemic Lupus Erythematosus |
| title_fullStr |
Epstein-Barr Virus and Systemic Lupus Erythematosus |
| title_full_unstemmed |
Epstein-Barr Virus and Systemic Lupus Erythematosus |
| title_sort |
epstein-barr virus and systemic lupus erythematosus |
| description |
The etiology of SLE is not fully established. SLE is a disease with periods of waning disease activity and intermittent flares. This fits well in theory to a latent virus infection, which occasionally switches to lytic cycle, and EBV infection has for long been suspected to be involved. This paper reviews EBV immunobiology and how this is related to SLE pathogenesis by illustrating uncontrolled reactivation of EBV as a disease mechanism for SLE. Studies on EBV in SLE patients show enlarged viral load, abnormal expression of viral lytic genes, impaired EBV-specific T-cell response, and increased levels of EBV-directed antibodies. These results suggest a role for reactivation of EBV infection in SLE. The increased level of EBV antibodies especially comprises an elevated titre of IgA antibodies, and the total number of EBV-reacting antibody isotypes is also enlarged. As EBV is known to be controlled by cell-mediated immunity, the reduced EBV-specific T-cell response in SLE patients may result in defective control of EBV causing frequent reactivation and expression of lytic cycle antigens. This gives rise to enhanced apoptosis and amplified cellular waste load resulting in activation of an immune response and development of EBV-directed antibodies and autoantibodies to cellular antigens. |
| publisher |
Hindawi Publishing Corporation |
| publishDate |
2012 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3395176/ |
| _version_ |
1611542627075751936 |