Abstract
APART from the specific anti-Epstein-Barr virus (EBV) response in infectious mononucleosis (IM), there is a strong general increase of antibody levels1. The major increase comprises IgM. As EBV has been shown to infect B lymphocytes selectively2 we hypothesised that the virus triggered the infected cells to release immunoglobulin, much like the effect of certain B-cell mitogens3, although the mechanism of activation must be different. It is known that EBV infection in vitro of human blood lymphocytes gives rise to increased DNA synthesis4 and that lymphoid cell lines carrying the EBV genome shed or release immunoglobulins5 of various classes. Furthermore, the IgM increase seen in IM would fit with a polyclonal B-cell activation (PBA) of EBV as PBA usually gives rise to IgM secretion6. To test this hypothesis, we have exposed lymphocytes from cord blood and adult peripheral blood to EBV in vitro and measured the released IgM, by a doubleantibody radioimmunoassay, and individual antibody-forming cells (PFC) against haptenated red blood cells and sheep red blood cells (SRBC).
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ROSÉN, A., GERGELY, P., JONDAL, M. et al. Polyclonal Ig production after Epstein-Barr virus infection of human lymphocytes in vitro. Nature 267, 52–54 (1977). https://doi.org/10.1038/267052a0
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DOI: https://doi.org/10.1038/267052a0
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