Modulation of Semliki Forest virus-induced infection of mice by defective-interfering virus.
Preparations of defective-interfering (DI) Semliki Forest virus (SFV) differed qualitatively in their ability to protect mice against lethal SFV-induced encephalitis. The preparations fell into three categories: (1) DI virus p13a protected the majority of mice and left them immune to subsequent challenge with 100 50% lethal doses of SFV; (2) DI virus p4 protected mice to a similar extent, but the susceptibility of all surviving mice to challenge suggested that the protection was mediated without the intervention of the adaptive immune response; and (3) DI virus p5 did not protect mice even though its interference titer was similar to that of the protective preparations. How DI viruses p4 and p13a modulate this lethal infection is not clear; the failure of p4 to stimulate protective immunity suggests that nonadaptive host responses are important, but neither p4 nor p13a altered the course of infection with a heterologous neurotropic virus. Compared with avirulent SFV infection, both DI virus-modulated infections were poorly immunogenic with regard to the humoral immune response, although a minority of mice did have high levels of neutralizing antibody. Other, unknown factors are evidently at work and remain to be elucidated.
D000818:Animals; D000914:Antibodies, Viral / Q000032:analysis; D000956:Antigens, Viral / Q000276:immunology; D003673:Defective Viruses / Q000502:physiology*; D008297:Male; D051379:Mice; D009500:Neutralization Tests; D012672:Semliki forest virus / Q000276:immunology / Q000502:physiology*; D014036:Togaviridae Infections / Q000276:immunology / Q000382:microbiology*; D014762:Viral Interference
D000914:Antibodies, Viral; D000956:Antigens, Viral