Defense mechanisms against bovine herpesvirus: relationship of virus-host cell events to susceptibility to antibody-complement cell lysis.
The interaction of infectious bovine rhinotracheitis virus and susceptible host cells was examined to determine whether an infected cell could be destroyed by humoral immune mechanisms before or after the transmission of virus to susceptible adjacent cells. Viral antigens were detectable on cell membranes at 6 h postinfection, but cells were not susceptible to antibody-complement lysis until 10 h postinfection. Intracellular infectious virus was also detectable at 10 h postinfection, and transmission to adjacent cells by the intracellular route began at this time. Extracellular virus was not detectable until 12 to 13 h postinfection. By the continual addition of antibody and complement, virus dissemination could be reduced more than 50-fold. These results support the hypothesis that the humoral immune mechanism may be involved in the recovery from herpesvirus infections.
D000818:Animals; D000914:Antibodies, Viral / Q000032:analysis; D000956:Antigens, Viral / Q000008:administration & dosage / Q000032:analysis; D002417:Cattle; D002418:Cattle Diseases / Q000276:immunology*; D003165:Complement System Proteins; D003588:Cytopathogenic Effect, Viral; D003601:Cytotoxicity Tests, Immunologic; D000939:Epitopes; D005455:Fluorescent Antibody Technique; D007109:Immunity; D066298:In Vitro Techniques; D007241:Infectious Bovine Rhinotracheitis / Q000276:immunology*; D007273:Injections, Intramuscular; D008297:Male; D011817:Rabbits; D013997:Time Factors
D000914:Antibodies, Viral; D000956:Antigens, Viral; D000939:Epitopes; D003165:Complement System Proteins