Antigenic variation among strains of rhinovirus type 51.
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Biomedical subjects
Publications and source records attributed to E J Stott.
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Cynomolgus macaques were vaccinated with inactivated simian immunodeficiency virus-infected cells and 'Quil-A' as adjuvant at 0, 4, 8, and 36 weeks or at 0, 4, 8, and 16 weeks. 2 weeks later these animals, together with a similar unvaccinated group, were challenged with 10 MID50 (50% monkey infectious doses) of a pool of SIVmac251 previously titrated in vivo. Virus was repeatedly isolated from unvaccinated animals on at least five separate occasions and proviral DNA was detected in circulating lymphocytes by polymerase chain reaction amplification. By contrast, virus and proviral DNA were not found in any of the vaccinated animals. However, the same vaccination regimen used after live virus challenge did not eliminate virus from previously infected macaques.
Attenuated simian immunodeficiency virus (SIV) induces potent protection against infection with wild-type virus, but the mechanism of this immunity remains obscure. Allogeneic antibodies, which arise within animals as a result of SIV infection, might protect against challenge with exogenous SIV grown in allogeneic cells. To test this hypothesis, eight macaques were infected with attenuated SIV and subsequently challenged with wild-type SIV grown in autologous cells or heterologous cells. The results clearly demonstrated that animals infected with attenuated SIV are protected against wild-type SIV grown in autologous or heterologous cells. Thus, the hypothesis that live attenuated SIV protects by the induction of allogeneic antibodies is not tenable.
Vaccination of cynomolgus macaques with beta-propiolactone inactivated SIVmacBK28 in Freund's adjuvant induced low but detectable levels of anti-SIV envelope (env) antibodies and T-cell responses and protected against challenge with the 32H isolate of SIVmac251 grown in C8166 cells. In contrast, purified recombinant SIV env and gag proteins derived from BK28 formulated in Syntex adjuvant generated consistent and long-lived cellular and humoral immune responses to SIV env, but failed to protect against infection with the 32H virus. Thus, protection against a heterogeneous challenge stock is possible by immunization with a molecularly-cloned virus, but not with recombinant proteins from the same molecular origin. High levels of anti-cell antibodies induced by the whole virus vaccine, but not by recombinant proteins, may have contributed to the protection observed.