Immunodetection of PrPSc in spleens of some scrapie-infected sheep but not BSE-infected cows.

Somerville, Robert A.; Birkett, Christopher R.; Farquhar, Christine; Hunter, Nora; Goldmann, Wilfred; Dornan, Jacqueline; Grover, Donald A.; Hennion, Ruth M.; Percy, C; Foster, James D.; Jeffrey, Martin

doi:10.1099/0022-1317-78-9-2389

Cited by 63 publications

(36 citation statements)

References 35 publications

(27 reference statements)

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“…However, to our knowledge only two natural cases of scrapie in a PrP AHQ /PrP AHQ sheep have been found in the United Kingdom in a flock where PrP ARQ is associated with highest susceptibility (M. Dawson, personal communication). This observation and the data for experimental challenge of sheep with the PrP AHQ allele show that this allele does not induce such an absolute resistance to TSEs as the PrP ARR allele (10,31). This seems to be consistent with the slightly increased in vitro conversion efficiencies of the PrP C_154H variant compared to the PrP C_171R variant in vitro (P different ϭ 0.06).…”

Section: Discussionsupporting

confidence: 75%

Susceptibility of Sheep for Scrapie as Assessed by In Vitro Conversion of Nine Naturally Occurring Variants of PrP

Bossers¹,

Vries²,

Smits³

2000

J Virol

114

112

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Section: Discussionsupporting

confidence: 75%

Susceptibility of Sheep for Scrapie as Assessed by In Vitro Conversion of Nine Naturally Occurring Variants of PrP

Bossers¹,

Vries²,

Smits³

2000

J Virol

114

112

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“…Sc and infectivity have not been found in the LRS, even though both are present in the peripheral and central nervous systems (Somerville et al, 1997;Wells et al, 1998). It is possible that the BSE agent can directly enter the autonomic nervous system without prior infection of the LRS following oral ingestion (McBride et al, 2001;Schulz-Schaeffer et al, 2000).…”

Section: Parallels In Natural Bse In Which Prpmentioning

confidence: 99%

Delay in onset of prion disease for the HY strain of transmissible mink encephalopathy as a result of prior peripheral inoculation with the replication-deficient DY strain

Bartz

Aiken

Bessen

2004

Journal of General Virology

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We report that the replication-deficient DY strain of transmissible mink encephalopathy (TME) can delay disease caused by the pathogenic HY TME strain. In this study, competition between the HY and DY TME agents was investigated following superinfection of the sciatic nerve and peritoneal cavity. Initially, DY TME infection was examined in the absence of superinfection and it was found that inoculation into the brain and sciatic nerve resulted in prion disease and PrP Sc deposition in brain but not lymphoreticular tissues. Conversely, intraperitoneal inoculation of the DY TME agent did not result in clinical symptoms, DY TME agent replication or PrP Sc deposition 400-600 days after infection. These findings indicate that the DY TME agent does not replicate in secondary lymphoid organs and is non-pathogenic when neuroinvasion is dependent on prior infection of the lymphoreticular system. However, intraperitoneal inoculation of the DY TME agent at 60 days, but not at 30 days, prior to intraperitoneal inoculation of the HY TME agent resulted in an extension of the HY TME incubation period. Inoculation of the DY TME agent into the sciatic nerve at 60 days prior to intrasciatic nerve inoculation of the HY TME agent did not delay the incubation period of HY TME. The ability of the DY TME agent to delay HY TME infection following extraneural inoculation, but not neural infection, suggests that HY and DY TME agent competition can occur in a common replication site whose cellular location precedes infection of both the lymphoreticular and peripheral nervous systems.

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“…In addition, we now have many different techniques to detect PrP Sc as a marker for scrapie infectivity [37,43,46,47,52,60]. In particular PrP Sc immunohistochemistry has been very useful in pathogenesis studies, as it offers the additional advantage of revealing the cellular and neuro-anatomical localization of PrP Sc in the tissues thereby providing valuable information on the neuroanatomical pathways.…”

Section: Introductionmentioning

confidence: 99%

TSE pathogenesis in cattle and sheep

2008

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-Many studies have been undertaken in rodents to study the pathogenesis of transmissible spongiform encephalopathies (TSE). Only a few studies have focused on the pathogenesis of bovine spongiform encephalopathy (BSE) and scrapie in their natural hosts. In this review, we summarize the most recent insights into the pathogenesis of BSE and scrapie starting from the initial uptake of TSE agents and crossing of the gut epithelium. Following replication in the gut-associated lymphoid tissues (GALT), TSE agents spread to the enteric nervous system (ENS) of the gut. Infection is then carried through the efferent fibers of the post-ganglionic neurons of the parasympathetic and sympathetic nervous system to the pre-ganglionic neurons in the medulla oblongata of the brain and the thoracic segments of the spinal cord. The differences between the pathogenesis of BSE in cattle and scrapie in sheep are discussed as well as the possible existence of additional pathogenetic routes.

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Immunodetection of PrPSc in spleens of some scrapie-infected sheep but not BSE-infected cows.

Cited by 63 publications

References 35 publications

Susceptibility of Sheep for Scrapie as Assessed by In Vitro Conversion of Nine Naturally Occurring Variants of PrP

Susceptibility of Sheep for Scrapie as Assessed by In Vitro Conversion of Nine Naturally Occurring Variants of PrP

Delay in onset of prion disease for the HY strain of transmissible mink encephalopathy as a result of prior peripheral inoculation with the replication-deficient DY strain

TSE pathogenesis in cattle and sheep

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