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The Journal of Experimental Medicine, Vol 133, 1074-1089, Copyright © 1971 by The Rockefeller University Press


ARTICLE

MECHANISMS OF RECOVERY FROM A GENERALIZED VIRAL INFECTION: MOUSEPOX : II. PASSIVE TRANSFER OF RECOVERY MECHANISMS WITH IMMUNE LYMPHOID CELLS



R. V. Blanden 1

1 From the Department of Microbiology, The John Curtin School of Medical Research, The Australian National University, Canberra, A.C.T., Australia

The following passive transfer experiments evaluated the contributions of the various host responses in recovery from mousepox. (a) Immune spleen cells transferred highly efficient antiviral activity, but preinfected recipients of these cells made no detectable splenic interferon or antibody in the 24 hr interval after cell transfer. (b) Passively administered interferon was ineffective. (c) Recipients of hyperimmune serum had much more antibody than recipients of immune spleen cells but significantly less antiviral activity. (d) Immune spleen cell populations with antiviral activity contained mediators of CMI to virus antigens. (e) The antiviral activity of immune spleen cells was specific; it was inhibited by in vitro treatment with ATS, anti-light chain serum, and anti-theta ascitic fluid, but not by removal of mononuclear phagocytes from the immune population.

These results are interpreted to mean that recovery mechanisms conferred by immune spleen cells were triggered by specifically sensitized, thymus-derived lymphocytes, and that antibody and interferon responses were of less importance. A radiosensitive recipient component was necessary for the full expression of the antiviral activity of both immune cells and immune serum. It seemed likely that this component was the blood monocyte.

Submitted on January 17, 1971


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