No reactivation of JCV and CMV infections in the temporal cortex and cerebellum of sporadic Creutzfeldt-Jakob disease patients
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No reactivation of JCV and CMV infections in the temporal cortex and cerebellum of sporadic Creutzfeldt-Jakob disease patients. / Löffler, Judith; Krasemann, Susanne; Zerr, Inga; Matschke, Jakob; Glatzel, Markus.
In: Am J Neurodegener Dis, Vol. 3, No. 3, 01.01.2014, p. 152-7.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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T1 - No reactivation of JCV and CMV infections in the temporal cortex and cerebellum of sporadic Creutzfeldt-Jakob disease patients
AU - Löffler, Judith
AU - Krasemann, Susanne
AU - Zerr, Inga
AU - Matschke, Jakob
AU - Glatzel, Markus
PY - 2014/1/1
Y1 - 2014/1/1
N2 - Sporadic Creutzfeldt-Jakob disease (sCJD) is characterized by great phenotypic variability regarding clinical course and neuropathology. The most prominent disease modifiers are a polymorphism in Codon 129 of the prion protein gene and conformational variations of the misfolded prion protein. The cellular form of the prion protein restricts replication of viruses and may be involved in viral host defense, and viral infections influence the presentation and neuropathology in prion diseased mice. We investigated the occurrence of reactivated persistent viral infections of the brain in brain tissue samples of 25 sCJD patients. No evidence of reactivated JCV and CMV infections could be detected. This suggests that JCV and CMV infections are not reactivated as consequence of prion disease and do not act as disease modifiers in sCJD.
AB - Sporadic Creutzfeldt-Jakob disease (sCJD) is characterized by great phenotypic variability regarding clinical course and neuropathology. The most prominent disease modifiers are a polymorphism in Codon 129 of the prion protein gene and conformational variations of the misfolded prion protein. The cellular form of the prion protein restricts replication of viruses and may be involved in viral host defense, and viral infections influence the presentation and neuropathology in prion diseased mice. We investigated the occurrence of reactivated persistent viral infections of the brain in brain tissue samples of 25 sCJD patients. No evidence of reactivated JCV and CMV infections could be detected. This suggests that JCV and CMV infections are not reactivated as consequence of prion disease and do not act as disease modifiers in sCJD.
M3 - SCORING: Journal article
C2 - 25628966
VL - 3
SP - 152
EP - 157
JO - Am J Neurodegener Dis
JF - Am J Neurodegener Dis
SN - 2165-591X
IS - 3
ER -