Transient Immunodeficiency During Asymptomatic Epstein-Barr Virus Infection

PEDIATRICS ◽  
1983 ◽  
Vol 71 (6) ◽  
pp. 964-967
Author(s):  
THOMAS J. BOWEN ◽  
RALPH J. WEDGWOOD ◽  
HANS D. OCHS ◽  
WERNER HENLE

In vivo and in vitro humoral and cellular immune responses were studied in a 2½-year-old girl immediately before, during, and after an asymptomatic infection with Epstein-Barr virus. During the acute EBV infection, the patient's peripheral blood mononuclear cells were deficient in immunoglobulin synthesis and suppressed the in vitro immunoglobulin synthesis of normal allogeneic cells. In vitro mitogen transformation of lymphocytes was reduced. In vivo antibody responses to the T cell-dependent antigens bacteriophage φX 174 and Keyhole limpet hemocyanin were markedly depressed. These studies suggest that suppressor cells induced during acute EBV infection not only suppress immunoglobulin synthesis in vitro, but also interfere with in vivo antibody synthesis.

1978 ◽  
Vol 148 (5) ◽  
pp. 1429-1434 ◽  
Author(s):  
L Slaughter ◽  
D A Carson ◽  
F C Jensen ◽  
T L Holbrook ◽  
J H Vaughan

Peripheral blood mononuclear cells from 10 patients with rheumatoid arthritis and 9 control subjects were cultured in vitro for 30 days with and without infection by Epstein-Barr virus. All cultures showed polyclonal stimulation of B cells as indicated by rising levels of IgM in the culture supernates, reaching maximal at 18-24 days, and with no quantitative or kinetic difference between the RA and control cells. IgM anti-IgG was also produced in both groups and maximally at 18-24 days, but in greater quantity by the RA lymphocytes. The anti-IgG made by the RA lymphocytes was more easily absorbed by solid phase IgG than was the anti-IgG made by the normal lymphocytes and thus was judged to be of higher affinity. RA lymphocytes uninfected with EBV had higher transformation scores than did the normal controls and developed spontaneously into permanent cell lines in six instances.


1994 ◽  
Vol 180 (5) ◽  
pp. 1995-1998 ◽  
Author(s):  
K Ritter ◽  
R J Kühl ◽  
F Semrau ◽  
H Eiffert ◽  
H D Kratzin ◽  
...  

Antibodies directed against the autoantigen p26 were detected in sera from 32 patients with acute Epstein-Barr virus (EBV) infection and clinical symptoms of infectious mononucleosis. P26 has now been identified as the enzyme manganese superoxide dismutase (MnSOD) by comparison of the NH2-terminal amino acid sequence. Antibodies against MnSOD belong to the immunoglobulin class M. They are not detectable in sera of patients with other herpesvirus infections. In the 32 patients investigated, the rise and fall of the autoantibodies coincides with the clinical symptoms. In vitro, the autoantibodies were shown to inhibit the dismutation of superoxide radicals by blocking MnSOD. As presented in the discussion this effect may contribute to the pathogenesis of acute EBV infection.


Biomolecules ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 38
Author(s):  
Christian Münz

The Epstein Barr virus (EBV) is one of the prominent human tumor viruses, and it is efficiently immune-controlled in most virus carriers. Cytotoxic lymphocytes strongly expand during symptomatic primary EBV infection and in preclinical in vivo models of this tumor virus infection. In these models and patients with primary immunodeficiencies, antibody blockade or deficiencies in certain molecular pathways lead to EBV-associated pathologies. In addition to T, NK, and NKT cell development, as well as their cytotoxic machinery, a set of co-stimulatory and co-inhibitory molecules was found to be required for EBV-specific immune control. The role of CD27/CD70, 4-1BB, SLAMs, NKG2D, CD16A/CD2, CTLA-4, and PD-1 will be discussed in this review. Some of these have just been recently identified as crucial for EBV-specific immune control, and for others, their important functions during protection were characterized in in vivo models of EBV infection and its immune control. These insights into the phenotype of cytotoxic lymphocytes that mediate the near-perfect immune control of EBV-associated malignancies might also guide immunotherapies against other tumors in the future.


1977 ◽  
Vol 146 (2) ◽  
pp. 495-508 ◽  
Author(s):  
D A Thorley-Lawson ◽  
L Chess ◽  
J L Strominger

Studies have been performed on in vitro infection by Epstein-Barr virus (EBV) of subpopulations of human lymphocytes. B cells of adult peripheral or fetal cord blood transform with equal efficiency, whether assayed by DNA synthesis induction or by outgrowth of transformed lymphocytes. In contrast, unfractionated adult lymphocytes transform much less efficiently than those from fetal cord. Reconstitution experiments of different cell preparations indicated that this difference was due to a suppression of B-cell proliferation by adult Ig-negative lymphocytes which fetal Ig-negative lymphocytes were unable to perform. Separation of Ig-negative lymphocytes into various subpopulations revealed that the suppression was performed by T cells. Macrophages and null cells play little or no role in suppression. The relevance of this phenomenon to infection and recovery from EBV infection during and after infectious mononucleosis is discussed.


2005 ◽  
Vol 79 (9) ◽  
pp. 5875-5879 ◽  
Author(s):  
Masanori Daibata ◽  
Kentaro Bandobashi ◽  
Masayuki Kuroda ◽  
Shosuke Imai ◽  
Isao Miyoshi ◽  
...  

ABSTRACT The purposeful induction of the lytic form of Epstein-Barr virus (EBV) infection combined with ganciclovir (GCV) treatment has been advocated as a novel strategy for EBV-positive B-cell lymphoma. We demonstrated that rituximab had a synergistic effect with dexamethasone on induction of the lytic EBV infection in CD20-positive lymphoma cells. Addition of GCV to the dexamethasone/rituximab-treated cells was more effective than dexamethasone/rituximab alone in killing EBV-positive lymphoma cells in vitro and in lymphoma-bearing nude mice but not in EBV-negative cells. These data suggest that induction of the lytic EBV infection with dexamethasone/rituximab in combination with GCV could be a potential virally targeted therapy for EBV-associated B-cell lymphoma.


Author(s):  
Olga S Fedyanina ◽  
Anna E Filippova ◽  
Olga I Demina ◽  
Olga A Zhuliabina ◽  
Dmitry S Tikhomirov ◽  
...  

Abstract Atypical mononuclear cells (AM) appear in significant numbers in peripheral blood of patients with Epstein-Barr virus (EBV)-associated infectious mononucleosis (IM). We investigated the number and lineage-specific clusters of differentiation (CD) expression of atypical mononuclear cells in 110 children with IM using the anti-CD antibody microarray for panning leukocytes by their surface markers prior to morphology examination. The AM population consisted primarily of CD8+ T cells with a small fraction (0%–2% of all lymphocytes) of CD19+ B lymphocytes. AM amount in children with mononucleosis caused by primary EBV infection was significantly higher than for IM caused by EBV reactivation or other viruses and constituted 1%–53% of all peripheral blood mononuclear cells compared to 0%–11% and 0%–8%, respectively. Children failing to recover from classic IM associated with primary EBV infection within 6 months had significantly lower percentage of CD8+ AM compared to patients with normal recovery rate.


2020 ◽  
Author(s):  
Mu-Sheng Zeng ◽  
li yan ◽  
Hua Zhang ◽  
Xiao-Dong Dong ◽  
Cong Sun ◽  
...  

Abstract Epstein-Barr virus (EBV), also known as the first human tumor virus, is linked to about 200,000 new cancer cases and millions of non-malignant diseases every year. EBV infects both human epithelial cells and B cells. Several virally encoded glycoproteins define tropism and mediate a complicated entry process. Here, we show that in both epithelial cells and B cells, R9AP silencing or genetic knockout significantly inhibits EBV infection, whereas R9AP overexpression promotes EBV infection, establishing R9AP as an essential entry receptor for EBV. Mechanistically, R9AP directly binds to EBV glycoproteins gH/gL to mediate membrane fusion. Importantly, the interaction of R9AP with gH/gL is inhibited by the highly potent, competitive gH/gL neutralizing antibody AMMO1 that blocks EBV infection of both epithelial cells and B cells. Furthermore, a R9AP peptide encompassing the gH/gL binding site inhibits EBV infection in vitro and reduces viral load in EBV infected humanized mice. Altogether, we propose R9AP as the first characterized receptor for EBV infection common to epithelial cells and B cells and a potential target for intervention.


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