Fred C . Jensen , Troy

There are two reasons for s tudying the possible role of the Epstein-Barr virus (EBV) in relation to rheumato id arthritis (RA). The first is the recent demonstrat ion by Alspaugh and co-workers that EBV infection o f normal peripheral blood lymphocytes induces the development in these cells of a nuclear antigen against which most patients with RA have precipitat ing antibodies (I). The second reason is that EBV is a natural ly occurring, polyclonal act ivator o f ant ibody product ion by h u m a n B lymphocytes (2, 3). In the present experiments, we have asked to what extent R A and normal subjects have B lymphoeytes which can be induced by EBV to secrete ant i-IgG antibodies. At the same time, we have determined the degree to which lymphoeytes from RA patients spontaneously transform in the absence of EBV infection. EBV nucleic acid can be detected in most permanent lines of h u m a n B cells (4). In most cases, therefore, EBV plays an essential role in the in vitro transformation of h u m a n B cells to permanent lines. I f R A lymphocytes undergo morphologic t ransformation and become permanent lines more readily than do normal lymphocytes, one might wonder whether or not they either contain more EBV genomes per cell than normal lymphocytes, or are abnormal ly responsive to EBV infection.