Inactivation of influenza B virus by normal guinea-pig serum.
Normal guinea-pig serum (GPS) lacking detectable antiviral antibody efficiently neutralized the infectivity of influenza B virus grown in chick embryos or MDCK cells. The inhibitor was heat-labile and sensitive to trypsin digestion. This beta-like inhibitor required Ca2+ and the complement components C1 and C4 for its activity. In contrast, GPS did not inactivate influenza A virus. Influenza B virus from which the neuraminidase activity of the spikes on the viral envelope had been eliminated by trypsin digestion was also inactivated to a level comparable to untreated virus. Complement component C1 alone bound directly to influenza B virus and inhibited its haemagglutinin activity. We suggest that the beta-like inhibitor in GPS is a component of the classical complement pathway which is triggered by the protein moiety of influenza B virus haemagglutinin, leading to virus neutralization.
D000818:Animals; D001790:Blood Physiological Phenomena; D002118:Calcium / Q000494:pharmacology; D003171:Complement Pathway, Classical; D003165:Complement System Proteins / Q000276:immunology; D006168:Guinea Pigs; D019267:Hemagglutinin Glycoproteins, Influenza Virus; D006389:Hemagglutinins, Viral / Q000032:analysis; D009981:Influenza B virus / Q000276:immunology*; D009500:Neutralization Tests; D015054:Zymosan / Q000494:pharmacology
D019267:Hemagglutinin Glycoproteins, Influenza Virus; D006389:Hemagglutinins, Viral; D003165:Complement System Proteins; D015054:Zymosan; D002118:Calcium