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Journal of Virology, January 2007, p. 689-697, Vol. 81, No. 2
0022-538X/07/$08.00+0     doi:10.1128/JVI.01751-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Prion Interference Is Due to a Reduction in Strain-Specific PrP^Sc Levels

Jason C. Bartz,^1* Michelle L. Kramer,¹ Meghan H. Sheehan,¹ Jessica A. L. Hutter,¹ Jacob I. Ayers,¹ Richard A. Bessen,³ and Anthony E. Kincaid²

Departments of Medical Microbiology and Immunology,¹ Physical Therapy, Creighton University, Omaha, Nebraska 68178,² Department of Veterinary Molecular Biology, Montana State University, Bozeman, Montana 59717³

Received 13 August 2006/ Accepted 19 October 2006

When two prion strains infect a single host, one strain can interfere with the ability of the other to cause disease but it is not known whether prion replication of the second strain is also diminished. To further investigate strain interference, we infected hamsters in the sciatic nerve with the long-incubation-period transmissible mink encephalopathy (TME) agent DY TME prior to superinfection of hamsters with the short-incubation-period HY TME agent. Increases in the interval between TME agent inoculations resulted in an extension of the incubation period of HY TME or a complete block of the ability of the HY TME agent to cause disease. The sciatic nerve route of inoculation gave the two TME strains access to the same population of neurons, allowing for the potential of prion interference in the lumbar spinal cord. The ability of the DY TME agent to extend the incubation period of HY TME corresponds with detection of DY TME PrP^Sc, the abnormal isoform of the prion protein, in the lumbar spinal cord. The increased incubation period of HY TME or the inability of the HY TME agent to cause disease in the coinfected animals corresponds with a reduction in the abundance of HY TME PrP^Sc in the lumbar spinal cord. When the two strains were not directed to the same populations of neurons within the lumbar spinal cord, interference between HY TME and DY TME did not occur. This suggests that DY TME agent replication interferes with HY TME agent replication when the two strains infect a common population of neurons.

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* Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, 2500 California Plaza, Omaha, NE 68178. Phone: (402) 280-1811. Fax: (402) 280-1875. E-mail: jbartz{at}creighton.edu.

Published ahead of print on 1 November 2006.

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Journal of Virology, January 2007, p. 689-697, Vol. 81, No. 2
0022-538X/07/$08.00+0     doi:10.1128/JVI.01751-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

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