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Effect of Selective Complement Deficiency on the Rate of Neutralization of Enveloped Viruses by Human Sera¹

From the Departments of Medicine and Microbiology, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642

Abstract

The capacity of human sera genetically deficient in selective complement (C) components to enhance neutralization of enveloped viruses was examined by kinetic plaque reduction assays. Vaccinia virus, a DNA virus, and vesicular stomatitis virus (VSV), an RNA virus, were studied. Exogenous rabbit or human antibody to vaccinia virus, and guinea pig or human antibody to VSV were provided in limiting, C-dependent concentrations. IgG antibodies predominated in most of the antisera employed.

C5-deficient and C6-deficient human sera consistently supported normal rates of neutralization of either virus; this effect was heat-labile. C4-deficient human serum did not exceed heat-inactivated serum in any neutralization assay. C1r-deficient serum displayed slight heat-labile neutralizing capacity against vaccinia but none against VSV. C2- and C3-deficient sera consistently exhibited measurable but clearly subnormal rates of neutralization. Two fresh agammaglobulinemic sera failed to inactivate either virus in the absence of added antibody.

These results confirm and extend earlier evidence, based on neutralization of herpes simplex and Newcastle disease viruses in the presence of early (IgM) antibody and functionally pure guinea pig C components or C-deficient animal sera, that the late-acting components C5–C9 are not required for C-dependent neutralization. Data on four enveloped viruses now agree that this function is mediated by C1–C3, although C1 plus C4 appear to have some neutralizing capacity. This requirement for C1–C3 is overcome, however, in the presence of higher antibody concentrations, suggesting that the contribution of the C system to viral neutralization in vivo may be chiefly in the early phase of infection when antibody is limited.

Footnotes

¹ This work was supported by research Grant AI-12568 and Training Grant AI-00028 from the United States Public Health Service, and by the David Welk Memorial Fund.