scholarly journals Epstein-Barr Virus and Systemic Lupus Erythematosus

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Anette Holck Draborg ◽  
Karen Duus ◽  
Gunnar Houen
Keyword(s):  
T Cell ◽  
Lupus Erythematosus ◽  
Cell Response ◽  
T Cell Response ◽  
Lytic Cycle ◽  
Cell Mediated Immunity ◽  
Barr Virus ◽  
Ebv Infection ◽  
Waste Load ◽  
Epstein Barr

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.

scholarly journals Primary Epstein-Barr virus infection does not erode preexisting CD8+ T cell memory in humans

2012 ◽  
Vol 209 (3) ◽  
pp. 471-478 ◽  
Author(s):  
Oludare A. Odumade ◽  
Jennifer A. Knight ◽  
David O. Schmeling ◽  
David Masopust ◽  
Henry H. Balfour ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Response ◽  
Epstein Barr Virus ◽  
Cd8 T Cell ◽  
T Cell Response ◽  
Epstein Barr Virus Infection ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr

Acute Epstein-Barr virus (EBV) infection results in an unusually robust CD8+ T cell response in young adults. Based on mouse studies, such a response would be predicted to result in attrition of preexisting memory to heterologous infections like influenza A (Flu) and cytomegalovirus (CMV). Furthermore, many studies have attempted to define the lymphocytosis that occurs during acute EBV infection in humans, but it is unclear whether bystander T cells contribute to it. To address these issues, we performed a longitudinal prospective study of primary EBV infection in humans. During acute EBV infection, both preexisting CMV- and Flu-specific memory CD8+ T cells showed signs of bystander activation, including up-regulation of granzyme B. However, they generally did not expand, suggesting that the profound CD8+ lymphocytosis associated with acute EBV infection is composed largely of EBV-specific T cells. Importantly, the numbers of CMV- and Flu-specific T cells were comparable before and after acute EBV infection. The data support the concept that, in humans, a robust CD8+ T cell response creates a new memory CD8+ T cell niche without substantially depleting preexisting memory for heterologous infections.

scholarly journals Epitope-specific Evolution of Human CD8+ T Cell Responses from Primary to Persistent Phases of Epstein-Barr Virus Infection

2002 ◽  
Vol 195 (7) ◽  
pp. 893-905 ◽  
Author(s):  
Andrew D. Hislop ◽  
Nicola E. Annels ◽  
Nancy H. Gudgeon ◽  
Alison M. Leese ◽  
Alan B. Rickinson
Keyword(s):  
T Cell ◽  
Virus Infection ◽  
Cell Response ◽  
Epstein Barr Virus ◽  
Cd8 T Cell ◽  
T Cell Response ◽  
Lytic Cycle ◽  
Phenotypic Change ◽  
Barr Virus ◽  
Epstein Barr

Primary virus infection often elicits a large CD8+ T cell response which subsequently contracts to a smaller memory T cell pool; the relationship between these two virus-specific populations is not well understood. Here we follow the human CD8+ T cell response to Epstein-Barr virus (EBV) from its primary phase in infectious mononucleosis (IM) through to the persistent carrier state. Using HLA-A2.1 or B8 tetramers specific for four lytic cycle and three latent cycle epitopes, we find marked differences in the epitope-specific composition of the T cell populations between the two phases of infection. The primary response is dominated by lytic epitope specificities which are severely culled (and in one case extinguished) with resolution of the acute infection; in contrast latent epitope specificities are less abundant, if present at all, in acute IM but often then increase their percentage representation in the CD8 pool. Even comparing epitopes of the same type, the relative size of responses seen in primary infection does not necessarily correlate with that seen in the longer term. We also follow the evolution of phenotypic change in these populations and show that, from a uniform CD45RA−RO+CCR7− phenotype in IM, lytic epitope responses show greater reversion to a CD45RA+RO− phenotype whereas latent epitope responses remain CD45RA−RO+ with a greater tendency to acquire CCR7. Interestingly these phenotypic distinctions reflect the source of the epitope as lytic or latent, and not the extent to which the response has been amplified in vivo.

scholarly journals Characterization of the CD4+ T Cell Response to Epstein-Barr Virus during Primary and Persistent Infection

2003 ◽  
Vol 198 (6) ◽  
pp. 903-911 ◽  
Author(s):  
Elisabeth Amyes ◽  
Chris Hatton ◽  
Damien Montamat-Sicotte ◽  
Nancy Gudgeon ◽  
Alan B. Rickinson ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Response ◽  
Cd4 T Cells ◽  
T Cell Response ◽  
Lytic Cycle ◽  
Cd4 T Cell ◽  
Barr Virus ◽  
Specific Effector ◽  
Epstein Barr

The CD8+ T cell response to Epstein-Barr virus (EBV) is well characterized. Much less is known about the evolution of the CD4+ T cell response. Here we show that EBV stimulates a primary burst of effector CD4+ T cells and this is followed by a period of down-regulation. A small population of EBV-specific effector CD4+ T cells survives during the lifelong persistent phase of infection. The EBV-specific effector CD4+ T cells accumulate within a CD27+ CD28+ differentiation compartment during primary infection and remain enriched within this compartment throughout the persistent phase of infection. Analysis of CD4+ T cell responses to individual epitopes from EBV latent and lytic cycle proteins confirms the observation that the majority of the effector cells express both CD27 and CD28, although CD4+ T cells specific for lytic cycle antigens have a greater tendency to express CD45RA than those specific for the latent antigens. In clear contrast, effector CD4+ T cells specific for cytomegalovirus (CMV) accumulate within the CD27− CD28+ and CD27− CD28− compartments. There are striking parallels in terms of the differentiation of CD8+ T cells specific for EBV and CMV. The results challenge current ideas on the definition of memory subsets.

scholarly journals Effect of methotrexate and anti-TNF on Epstein-Barr virus T-cell response and viral load in patients with rheumatoid arthritis or spondylarthropathies

2009 ◽  
Vol 11 (3) ◽  
pp. R77 ◽  
Author(s):  
Corinne Miceli-Richard ◽  
Nicolas Gestermann ◽  
Corinne Amiel ◽  
Jérémie Sellam ◽  
Marc Ittah ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Viral Load ◽  
T Cell ◽  
Cell Response ◽  
Epstein Barr Virus ◽  
T Cell Response ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Cytolytic T-cell response against Epstein-Barr virus in lung cancer patients and healthy subjects

2010 ◽  
Vol 29 (1) ◽  
Author(s):  
Vaios Karanikas ◽  
Maria Zamanakou ◽  
Faye Soukou ◽  
Theodora Kerenidi ◽  
Ioannis Tsougos ◽  
...  
Keyword(s):  
Lung Cancer ◽  
T Cell ◽  
Cancer Patients ◽  
Cell Response ◽  
Healthy Subjects ◽  
Epstein Barr Virus ◽  
T Cell Response ◽  
Lung Cancer Patients ◽  
Barr Virus ◽  
Epstein Barr

EPSTEIN-BARR VIRUS-SPECIFIC CYTOTOXIC T CELL RESPONSE IN CARDIAC TRANSPLANT RECIPIENTS

1994 ◽  
Vol 57 (11) ◽  
pp. 1611-1616
Author(s):  
Myat T. Kyaw-Tanner ◽  
Donald Esmore ◽  
Scott R. Burrows ◽  
Elizabeth M. Benson ◽  
Tom B. Sculley
Keyword(s):  
T Cell ◽  
Cell Response ◽  
Epstein Barr Virus ◽  
T Cell Response ◽  
Cytotoxic T Cell ◽  
Cardiac Transplant ◽  
Transplant Recipients ◽  
Barr Virus ◽  
Epstein Barr

Interleukin-10 expression and cytotoxic-T-cell response in Epstein-Barr-virus-associated nasopharyngeal carcinoma

1997 ◽  
Vol 72 (3) ◽  
pp. 398-402 ◽  
Author(s):  
Min Yao ◽  
Koichi Ohshima ◽  
Junji Suzumiya ◽  
Tohru Kume ◽  
Toyo-o Shiroshita ◽  
...  
Keyword(s):  
T Cell ◽  
Nasopharyngeal Carcinoma ◽  
Cell Response ◽  
Epstein Barr Virus ◽  
Interleukin 10 ◽  
T Cell Response ◽  
Cytotoxic T Cell ◽  
Barr Virus ◽  
Epstein Barr

Immunodominant CD8 T cell response to Epstein-Barr virus

2001 ◽  
Vol 55 (7) ◽  
pp. 373-380 ◽  
Author(s):  
E Houssaint ◽  
X Saulquin ◽  
E Scotet ◽  
M Bonneville
Keyword(s):  
T Cell ◽  
Cell Response ◽  
Epstein Barr Virus ◽  
Cd8 T Cell ◽  
T Cell Response ◽  
Barr Virus ◽  
Epstein Barr

Oligopeptide Induction of a Secondary Cytotoxic T-cell Response to Epstein-Barr Virus In Vitro

1991 ◽  
Vol 33 (4) ◽  
pp. 411-420 ◽  
Author(s):  
C. SCHMIDT ◽  
S. R. BURROWS ◽  
D. J. MOSS ◽  
T. B. SCULLEY ◽  
I. S. MISKO
Keyword(s):  
T Cell ◽  
Cell Response ◽  
Epstein Barr Virus ◽  
T Cell Response ◽  
Cytotoxic T Cell ◽  
Barr Virus ◽  
Epstein Barr
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