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Table 1
Features of TSE diseases for which the RuNAway model may provide an explanation
TSE Feature	Explanation afforded by RuNAway

Endogenous origin of TSE	SINEs are endogenous
TSE Agent becomes infectious	TSE causing SINE is mutated for enhanced replication
	and virulence
Long latency	RT-mediated SINE gene proliferation is a slow
	process. Spreading between cells is much less efficient
	than viral infection
Shorter visible disease period	Transition to aggressive second RuNAway cycle
Inheritance of TSE strain	SINEs are nucleic acid and obey the laws of genetics
variation	and inheritance
Species barrier to infection	Adaptation to new RNA primer sequence required in
	new host species
Absence of immune reaction	SINEs are nucleic acid and therefore not immunogenic
PrP protein required for	When overproduced, PrP protein is prone to form
pathology	aggregates which damage neighbouring cells
Agent causes PrP^Sc precipitation	SINEs can inhibit PKR a negative regulator of
	translation, leading to overproduction of PrP protein
	and deposition of amyloid plaques
PrP^0/0 mouse does not succumb	PrP^0/0 mouse is infected by scrapie SINEs but without
to scrapie	PrP expression no amyloid plaques can form
PrP^0/0 mouse transmits scrapie	TSE SINE replicates in PrP^0/0 mouse cells
agent
PrP^0/0 mouse transmits scrapie	TSE SINE replication is dependent on SINE RNA
agent less efficiently than	synthesis which is not stress-induced in the absence of
wildtype mouse	second RuNAway cycle

Gibson Genome Biology 2001 2:preprint0006.1 doi:10.1186/gb-2001-2-7-preprint0006

Table 1