Impaired Epstein-Barr Virus-Specific Neutralizing Antibody Response during Acute Infectious Mononucleosis Is Coincident with Global B-Cell Dysfunction

Here we present evidence for previously unappreciated B-cell immune dysregulation during acute Epstein-Barr virus (EBV)-associated infectious mononucleosis (IM). Longitudinal analyses revealed that patients with acute IM have undetectable EBV-specific neutralizing antibodies and gp350-specific B-cel...

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Bibliographic Details
Published in:Journal of virology 2015-09, Vol.89 (17), p.9137-9141
Main Authors: Panikkar, Archana, Smith, Corey, Hislop, Andrew, Tellam, Nick, Dasari, Vijayendra, Hogquist, Kristin A, Wykes, Michelle, Moss, Denis J, Rickinson, Alan, Balfour, Jr, Henry H, Khanna, Rajiv
Format: Article
Language:English
Subjects:
Antibodies, Neutralizing - immunology
Antibodies, Viral - immunology
B-Cell Activating Factor - immunology
B-Lymphocytes - immunology
B-Lymphocytes - virology
Capsid Proteins - immunology
CD8-Positive T-Lymphocytes - immunology
Epstein-Barr Virus Infections - immunology
Epstein-Barr Virus Infections - virology
fas Receptor - metabolism
Herpesvirus 4, Human - immunology
Humans
Immunologic Memory - immunology
Infectious Mononucleosis - immunology
Infectious Mononucleosis - virology
Lymphocyte Activation - immunology
Pathogenesis and Immunity
Tumor Necrosis Factor Ligand Superfamily Member 13 - immunology
Viral Matrix Proteins - immunology
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Summary:Here we present evidence for previously unappreciated B-cell immune dysregulation during acute Epstein-Barr virus (EBV)-associated infectious mononucleosis (IM). Longitudinal analyses revealed that patients with acute IM have undetectable EBV-specific neutralizing antibodies and gp350-specific B-cell responses, which were associated with a significant reduction in memory B cells and no evidence of circulating antibody-secreting cells. These observations correlate with dysregulation of tumor necrosis factor family members BAFF and APRIL and increased expression of FAS on circulating B cells.
ISSN:0022-538X
1098-5514
DOI:10.1128/JVI.01293-15