It has been observed that certain laboratory models-- rabbits and few others developed spontaneous neurological symptoms upon inoculation with infectious Prion strains, could Murine Endogenous Retroviruses be the cause or consequence of these observed neurological symptoms?
This is a truly intriguing hypothesis. Some of the erv particles are quite immunogenic. I guess you could go to the bottom of your excellent question by inoculating tg mice that lack erv sequences
That is also a possibility. My point was to see what happens with the degree of prion transmission. Is it more attenuated in the null mice? Since ervs are immunogenic chances are that a greater cytokine cascade will facilitate transmission in a way.
It is true that so far there is evidence of a causative association between activation of ERV sequences and disease in humans. However, in subsets of patients with MS and schizophrenia these sequences are expressed. Whether this is an epiphenomenon or not remains unclear. It is odd that this HERV activation is specific for a disease (HERV-W in MS). Polymorphisms in this gene increase your risk of MS. ERVS play also a functional role in the human genome. For instance syncytin is originally a retrovirus gene that became integrated in our genome. Syncytin is crucial for placenta development. There are concerns about xenograft transplants and transmission of other mammal ERVs to humans.
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