10.5061/DRYAD.7PVMCVDWN
Karsten, Christina
University of Duisburg-Essen
Bartsch, Yannic
Ragon Institute of MGH, MIT and Harvard
Shin, Sally
Ragon Institute of MGH, MIT and Harvard
Slein, Matthew
Ragon Institute of MGH, MIT and Harvard
Heller, Howard
Massachusetts Institute of Technology
Kolandaivelu, Kumaran
Massachusetts Institute of Technology
Middeldorp, Jaap
Amsterdam University Medical Centers
Alter, Galit
Ragon Institute of MGH, MIT and Harvard
Julg, Boris
0000-0002-4687-9626
Ragon Institute of MGH, MIT and Harvard
Data from: Evolution of functional antibodies following acute Epstein-Barr
Virus infection
Dryad
dataset
2022
FOS: Medical and health sciences
Ragon Institute of MGH, MIT and Harvard
https://ror.org/053r20n13
2022-08-25T00:00:00Z
2022-08-25T00:00:00Z
en
3110014 bytes
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CC0 1.0 Universal (CC0 1.0) Public Domain Dedication
While Epstein-Barr virus causes mostly asymptomatic infection, associated
malignancies, and autoimmune and lymphoproliferative diseases occur. To
dissect the evolution of humoral immune responses over the course of EBV
infection and to gain a better understanding of the potential contribution
of antibody (Ab) function to viral control, we comprehensively profiled Ab
specificities and Fc-functionalities using systems serology and VirScan.
Ab functions against two early (p18 and p47/54) and two latent (gp350/220
and EBNA-1) EBV proteins were overall modest and/or short-lived, differing
from humoral responses induced during acute infection by other viruses
such as HIV. In the first year post-infection, only p18 elicited robust
IgM-driven complement deposition and IgG-driven neutrophil phagocytosis
while responses against EBNA-1 were largely Fc-functionally silent and
only matured during chronic infection to drive phagocytosis. In contrast,
Abs against Influenza virus readily mediated broad Fc-activity in all
participants. These data suggest that EBV evades the induction of robust
Fc-functional Abs, potentially due to the virus’ life cycle, switching
from lytic to latent stages during infection.
SOI scoring was used to determine the severity of illness. ELISAs were
used to confirm EBV status, the titer, and class/subclass of EBV-specific
antibodies. qPCR was used to determine viral load. High-throughput flow
cytometry techniques of the systems serology pipeline were used to assess
antibody-mediated immune functions. Luminex assays were used to determine
antibody binding to Fc receptors. Antibody depletion experiments were used
to test suspected causal associations between specific antibody classes
and functions. Virscan analysis was used to determine the breadth of
existing and evolving antibody responses.
Prism, Excel.