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The Effect of Antibody on Rubella Virus Infection in Human Lymphoid Cells

Division of Medical Microbiology, University of British Columbia, Vancouver, British Columbia, Canada V6T 1W5

The effect of rabbit anti-rubella virus (RV) serum on the course of RV infection of human lymphoid cells has been examined. The antibody was found to abolish viral replication such that no virus progeny could be detected either extracellularly (after removal of the antiserum) or intracellularly, in the treated cells. Viral protein synthesis was also found to be totally inhibited in the presence of anti-RV but resumed immediately on removal of the antibody block at levels suggesting that viral RNA had been accumulating in the cell. Infectious focus assays indicated that the effect could be explained in part by the restriction by antiviral antibody of cell-to-cell spread in the indicator monolayer. Thus by 48 h when 100% of lymphoid cells infected with virus alone were capable of forming infectious foci, only 40 to 50% of cells infected in the presence of antiviral antibody produced foci. However this restriction imposed by antibody did not adequately explain the total inhibition of viral protein synthesis that occurred under these conditions. Pretreatment of RV with excess neutralizing antiserum reduced the virus titre > 99.9% but did not eliminate infectious virus. The ‘non-neutralized’ fraction (10² to 10³ p.f.u./ml) brought about a productive infection with final yields of 10 to 25% of control titres (> 10⁵ p.f.u./ml). Incubation of virus with both anti-RV and goat anti-rabbit Ig eliminated viral infectivity, indicating that the ‘non-neutralized’ fraction was in the form of infectious immune complexes. The results suggest two major modes of action for anti-RV antibody, one in neutralizing extracellular virus, the second exerted on the infected cells, totally inhibiting viral translation and thus preventing the virus from completing its replicative cycle.

Keywords: rubella virus, antibody, lymphoid cells

Received 21 October 1986; accepted 8 January 1987.