ArticleProceedings of the National Academy of Sciences of the United States of America1998
Vaccination with an attenuated Creutzfeldt-Jakob disease strain prevents expression of a virulent agent.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 73 citations in OpenAlex.
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- Agent-specific Shadoo responses in transmissible encephalopathies.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2010Article
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1 author at 1 institution in 1 country.
Funding
Abstract
Although slow and persistent viruses often escape host defenses infection may be prevented by live vaccines. To determine whether an attenuated "slow" strain of the Creutzfeldt-Jakob disease agent (SY) could block expression of a virulent "fast" strain (FU), outbred CD-1 mice were inoculated intracerebrally with low infectious doses of SY and challenged 80 days later with higher doses of FU. For comparison, the same SY and FU samples were inoculated in two parallel control groups. All 18 superinfected mice showed incubation times identical to those inoculated with only the SY strain, yielding clinical disease >110 days later than predicted for the FU strain. Neurological signs, such as scratching and an extended clinical phase, were also characteristic for SY but not FU infection. Moreover, the widespread cortical pathology of FU was not detectable in superinfected mice. Western blot analyses further showed no strain-specific differences in prion protein (PrP) band profiles for all experimental groups, although there was approximately 10-fold more protease-resistant PrP (PrP-res) in FU brains during terminal disease. In contrast, infectivity assays revealed an approximately 10,000-fold difference between SY and FU at terminal stages, indicating that PrP-res content does not correlate with infectivity. In summary, an attenuated strain of the Creutzfeldt-Jakob disease agent evokes substantial interference against a virulent agent. Because superinfected mice had little PrP-res just before the onset of clinical disease and retained abundant cellular PrP, cellular PrP was not the factor limiting FU replication. The mechanisms underlying SY interference are not understood but could be based on host recognition of foreign molecular features shared by this class of invasive agents involving antibody production, and possibly involve defective viral particles produced by attenuated variants.
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