It is good to see more data on the complex host responses to different TSE strains. Readers may also be interested in our 2004 paper on new molecular markers of early and progressive CJD infection (ZY Lu, CA Baker and L Manuelidis: J Cell Biochem 93:644-652, 2004). In that study, significant >10 fold elevations of innate immuity genes were apparent by 30 days in CJD but not mock inoculated brains by RT-PCR. These changes were evident 60 days before the appearance of pathological PrP. Because these early responses appeared to be specific only for one of two different CJD isolates, we suggested that particular host markers could be used to distinguish among individual TSE strains.
The current study of other host genes in 3 additional scrapie strains further substantiates the concept of differential host responses to individual TSE strains. Specific strain dependent responses to infection may arise, at least in part, from agents that target different cell types in the brain and/or that have a preference for different intracellular compartments. These compartments may not coincide with those involved in PrP metabolism.
Competing interests
I have a PCT application PCT/US2005/007189 filed March 4, 2005 entitled "Presymptomatic markers for disease associated with Transmissible Encephalopathies"
Strain specific markers in TSEs
26 May 2006
It is good to see more data on the complex host responses to different TSE strains. Readers may also be interested in our 2004 paper on new molecular markers of early and progressive CJD infection (ZY Lu, CA Baker and L Manuelidis: J Cell Biochem 93:644-652, 2004). In that study, significant >10 fold elevations of innate immuity genes were apparent by 30 days in CJD but not mock inoculated brains by RT-PCR. These changes were evident 60 days before the appearance of pathological PrP. Because these early responses appeared to be specific only for one of two different CJD isolates, we suggested that particular host markers could be used to distinguish among individual TSE strains.
The current study of other host genes in 3 additional scrapie strains further substantiates the concept of differential host responses to individual TSE strains. Specific strain dependent responses to infection may arise, at least in part, from agents that target different cell types in the brain and/or that have a preference for different intracellular compartments. These compartments may not coincide with those involved in PrP metabolism.
Competing interests
I have a PCT application PCT/US2005/007189 filed March 4, 2005 entitled "Presymptomatic markers for disease associated with Transmissible Encephalopathies"