作者: Toby J Gibson
DOI: 10.1186/GB-2001-2-7-PREPRINT0006
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摘要: Despite decades of research, the agent responsible for transmitting spongiform encephalopathies (TSEs) has not been identified. The Prion hypothesis, which dominates field, supposes that modified host PrP protein, termed PrPSc, acts as transmissible agent. This model fits observation TSE diseases elicit almost no immune reaction. transmission verified, however, it possible to produce pure PrPSc aggregates. One long-standing objection is disease agents show classical genetic behaviours, such reproducible strain variation, while also responding selection novel traits adaptation new hosts. Moreover, evidence steadily accumulating infectious titre decoupled from quantity (or even presence) deposits. Rather awkwardly PrP0/0 knockout mice have found incubate and transmit (despite themselves being refractory disease). In this article, a scheme, RuNAway, proposed whereby uncontrolled proliferation type parasitic gene, small dispersed repeat sequences (SINEs), in somatic cells induces overproduction with pathogenic consequences. RuNAway scheme involves twin tandem positive feedback loops: triggering second loop leads disease. consistent long latency period much shorter visible progression typical TSEs.