Mad cow disease without the prions

[rathelios]

...suggests alternative vector such as a virus.

New Scientist article shows disease without presence of prions.

Whereas this paper shows presence of prions without disease.

The 1997 Nobel Physiology Prize went to Stanley Prusiner for his work in demonstrating that prions cause spongiform encephalopathy diseases such as:
Human prion diseases:
Variant Creutzfeldt-Jakob Disease (vCJD)
Gerstmann-Straussler-Scheinker Syndrome
Fatal Familial Insomnia
Kuru
Animal Prion Diseases:
Bovine Spongiform Encephalopathy (BSE)
Chronic Wasting Disease (CWD)
Scrapie
Transmissible mink encephalopathy
Feline spongiform encephalopathy
Ungulate spongiform encephalopathy

In a nutshell (lol) the theory being that abnormally shaped proteins (called prions) catalyse other proteins to change shape and also become prions and thus cause the disease. They are apparently transmissible to other organisms, even other species, where they catalyse other proteins to change shape in the same way.
Explained in more detail here for those of a scientific bent.

This latest bombshell from the New Scientist article in which mice were infected and promptly died but did not show much, or in some cases any, evidence of prions is potentially huge.
If these results are replicated expect more on this story in years to come and much egg on the faces of lots of people in the scientific establishment.

[The Fish]

The issue is that not all prions are equal. In the PNAS article you cited, the issue was that different isoforms of the PrpPSc protein had different transmissibility characteristics. The fact remains, though, that spongiform encephalopathies can still be transmitted by prions, but not all prions can do so equally. I can't really speak to the first article, but it is quite possible that the prion isotype used in the study had variant transmissibility characteristics that prevented disease (as the second article noted, some PrPSc variants apparently cause amyloid plaques without actual spongiform lesions).
In any case, I don't think this will turn anything on its head; it simply confirms that, just as with any infectious agents, there are different "strains" of prion proteins that interact with human proteins in a myriad of ways, resulting in varied clinical outcomes.

Very interesting articles!