Abstract
Abstract
Human fibroblast interferon (HFIF) and human leukocyte interferon (HLIF) can protect mouse L-929 cells against the cytopathic effects of vesicular stomatitis virus (VSV), although HLIF is about 60 times and HFIF about 1200 times less active than mouse interferon (MIF). This relationship suggests that, with repsect to the mouse L-929 receptor, there exists a greater similarity between the active sites of MIF and HLIF than between MIF and HFIF. Employing antibodies directed against MIF, HFIF, and HLIF as a probe, we found interferon-cell interactions to be stronger for homologous than for heterologous combinations. A variable-fit model is proposed to explain the differences that interferons display in cross-species protection. Thus, the closer the fit between interferon and receptor, the greater the antiviral response.
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