Absence of Requirement of Complement Activation for Recovery from Virus Infection

Abstract

Abstract Herpes simplex virus (HSV) neutralization by antibody, in vitro, is enhanced by activation of the classical complement pathway (C1,4,2 and 3). This study was designed to test the importance of this mechanism in vivo. Groups of normal Hartley guinea pigs (GP) and GP genetically deficient in the fourth component of complement (C4D) were infected with HSV by either the intradermal (i.d.) or i.p. route and intranasally with parainfluenza virus, type 3 (Pf3). General condition was monitored and viral cultures were obtained periodically. Multiple blood samples were obtained by cardiac puncture for determining CH50 and specific activities of C1, C4, and the C3–9 complex, as well as viral antibody. After i.d. infection with HSV, skin lesion biopsies from normal GP were positive for virus through day 6. CH50, C1, C4, and C3–9 complex activities did not differ from those of sham-injected controls. Intranasal Pf3 inoculation in normal GP resulted in hoarseness and lethargy.