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J. Virol., 02 1995, 734-740, Vol 69, No. 2
MB Goldman, TA O'Bryan, DJ Buckthal, LM Tetor and JN Goldman
Immune regulation of measles virus (MV) expression was studied in a
persistently infected mouse macrophage cell line. Synthesis of both
membrane-associated and internal MV antigens was suppressed when infected
macrophages were treated with polyclonal rabbit anti-MV antibody that was
specific for MV proteins. Persistently infected macrophages were treated
for 3, 5, or 7 days with increasing doses of anti-MV antibody. All MV
proteins were down-regulated 2 days after treatment was terminated. One
week after treatment was terminated, down- regulation was still evident but
to a lesser degree. MV protein synthesis was suppressed whether or not
complement components were inactivated by heating all serum supplements and
antibodies. However, when complement was active, cell lysis accounted for
some of the reduced MV protein synthesis. When lytic destruction of
infected cells by antibody and complement was prevented by inactivation of
complement, antibody alone reduced the cellular synthesis of viral proteins
by noncytolytic mechanisms. The absence of cell death in the absence of
complement was confirmed by the lack of 51Cr release from labeled cells,
the lack of reduction in cell number, and the lack of a decrease in total
protein synthesis when radiolabeled infected cells were treated with
antibody. It is noteworthy that low doses of antibody were optimal for
suppression in the longer-term experiments and did not cause lysis, even in
the presence of active complement. Since infected macrophages disseminate
virus in measles infection, noncytolytic regulation of these cells by
antibody may supplement viral clearance by cytolytic T cells and other
immune mechanisms.
Copyright © 1995, American Society for Microbiology
Suppression of measles virus expression by noncytolytic antibody in an immortalized macrophage cell line
Department of Medicine, Pennsylvania State University, Hershey 17033.
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