Abstract
The host response to viral infection may include stimulation of humoral and cellular immune mechanisms and interferon production. Whether these are causally related or are merely temporally associated with recovery from viral infection remains uncertain partly because of the nature of available evidence (1, 2). Recently we reported that a new specific viral resistance factor called serum protective factor (SPF) played the major role in recovery from primary Langat virus infection and cross-protection with arboviruses in mice in contrast to the insignificant roles of in vivo-produced neutralizing antibody and interferon (3–5). SPF can be distinguished from interferon (3, 4) by a) lability at pH 3.0 after 3 hr at 4°C, b) lability on dialysis against distilled water, c) specific activity in providing protection against very closely related viruses, d) persistence for at least 3 weeks following viral infection, and e) failure of in vivo production when mice are inoculated with inactivated viruses.

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