Co-infection with the friend retrovirus and mouse scrapie does not alter prion disease pathogenesis in susceptible mice.
Prion diseases are fatal, transmissible neurodegenerative diseases of the central nervous system. An abnormally protease-resistant and insoluble form (PrP(Sc)) of the normally soluble protease-sensitive host prion protein (PrP(C)) is the major component of the infectious prion. During the course of...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2012-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3266293?pdf=render |
| _version_ | 1818381754144129024 |
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| author | Pascal Leblanc Kim Hasenkrug Anne Ward Lara Myers Ronald J Messer Sandrine Alais Andrew Timmes Suzette A Priola |
| author_facet | Pascal Leblanc Kim Hasenkrug Anne Ward Lara Myers Ronald J Messer Sandrine Alais Andrew Timmes Suzette A Priola |
| author_sort | Pascal Leblanc |
| collection | DOAJ |
| description | Prion diseases are fatal, transmissible neurodegenerative diseases of the central nervous system. An abnormally protease-resistant and insoluble form (PrP(Sc)) of the normally soluble protease-sensitive host prion protein (PrP(C)) is the major component of the infectious prion. During the course of prion disease, PrP(Sc) accumulates primarily in the lymphoreticular and central nervous systems. Recent studies have shown that co-infection of prion-infected fibroblast cells with the Moloney murine leukemia virus (Mo-MuLV) strongly enhanced the release and spread of scrapie infectivity in cell culture, suggesting that retroviral coinfection might significantly influence prion spread and disease incubation times in vivo. We now show that another retrovirus, the murine leukemia virus Friend (F-MuLV), also enhanced the release and spread of scrapie infectivity in cell culture. However, peripheral co-infection of mice with both Friend virus and the mouse scrapie strain 22L did not alter scrapie disease incubation times, the levels of PrP(Sc) in the brain or spleen, or the distribution of pathological lesions in the brain. Thus, retroviral co-infection does not necessarily alter prion disease pathogenesis in vivo, most likely because of different cell-specific sites of replication for scrapie and F-MuLV. |
| first_indexed | 2024-12-14T02:39:36Z |
| format | Article |
| id | doaj.art-90b6cdac11064e1aa166da223f530f4a |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-14T02:39:36Z |
| publishDate | 2012-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-90b6cdac11064e1aa166da223f530f4a2022-12-21T23:20:02ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-0171e3087210.1371/journal.pone.0030872Co-infection with the friend retrovirus and mouse scrapie does not alter prion disease pathogenesis in susceptible mice.Pascal LeblancKim HasenkrugAnne WardLara MyersRonald J MesserSandrine AlaisAndrew TimmesSuzette A PriolaPrion diseases are fatal, transmissible neurodegenerative diseases of the central nervous system. An abnormally protease-resistant and insoluble form (PrP(Sc)) of the normally soluble protease-sensitive host prion protein (PrP(C)) is the major component of the infectious prion. During the course of prion disease, PrP(Sc) accumulates primarily in the lymphoreticular and central nervous systems. Recent studies have shown that co-infection of prion-infected fibroblast cells with the Moloney murine leukemia virus (Mo-MuLV) strongly enhanced the release and spread of scrapie infectivity in cell culture, suggesting that retroviral coinfection might significantly influence prion spread and disease incubation times in vivo. We now show that another retrovirus, the murine leukemia virus Friend (F-MuLV), also enhanced the release and spread of scrapie infectivity in cell culture. However, peripheral co-infection of mice with both Friend virus and the mouse scrapie strain 22L did not alter scrapie disease incubation times, the levels of PrP(Sc) in the brain or spleen, or the distribution of pathological lesions in the brain. Thus, retroviral co-infection does not necessarily alter prion disease pathogenesis in vivo, most likely because of different cell-specific sites of replication for scrapie and F-MuLV.http://europepmc.org/articles/PMC3266293?pdf=render |
| spellingShingle | Pascal Leblanc Kim Hasenkrug Anne Ward Lara Myers Ronald J Messer Sandrine Alais Andrew Timmes Suzette A Priola Co-infection with the friend retrovirus and mouse scrapie does not alter prion disease pathogenesis in susceptible mice. PLoS ONE |
| title | Co-infection with the friend retrovirus and mouse scrapie does not alter prion disease pathogenesis in susceptible mice. |
| title_full | Co-infection with the friend retrovirus and mouse scrapie does not alter prion disease pathogenesis in susceptible mice. |
| title_fullStr | Co-infection with the friend retrovirus and mouse scrapie does not alter prion disease pathogenesis in susceptible mice. |
| title_full_unstemmed | Co-infection with the friend retrovirus and mouse scrapie does not alter prion disease pathogenesis in susceptible mice. |
| title_short | Co-infection with the friend retrovirus and mouse scrapie does not alter prion disease pathogenesis in susceptible mice. |
| title_sort | co infection with the friend retrovirus and mouse scrapie does not alter prion disease pathogenesis in susceptible mice |
| url | http://europepmc.org/articles/PMC3266293?pdf=render |
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