PortalPublikationenNo reactivation of JCV and CMV infections in the temporal co...

No reactivation of JCV and CMV infections in the temporal cortex and cerebellum of sporadic Creutzfeldt-Jakob disease patients

Standard

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, Jahrgang 3, Nr. 3, 01.01.2014, S. 152-7.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Löffler, J, Krasemann, S, Zerr, I, Matschke, J & Glatzel, M 2014, 'No reactivation of JCV and CMV infections in the temporal cortex and cerebellum of sporadic Creutzfeldt-Jakob disease patients', Am J Neurodegener Dis, Jg. 3, Nr. 3, S. 152-7.

APA

Löffler, J., Krasemann, S., Zerr, I., Matschke, J., & Glatzel, M. (2014). No reactivation of JCV and CMV infections in the temporal cortex and cerebellum of sporadic Creutzfeldt-Jakob disease patients. Am J Neurodegener Dis, 3(3), 152-7.

Vancouver

Löffler J, Krasemann S, Zerr I, Matschke J, Glatzel M. No reactivation of JCV and CMV infections in the temporal cortex and cerebellum of sporadic Creutzfeldt-Jakob disease patients. Am J Neurodegener Dis. 2014 Jan 1;3(3):152-7.

Bibtex

@article{3234370bb8fa4242b3db143bd437da34,
title = "No reactivation of JCV and CMV infections in the temporal cortex and cerebellum of sporadic Creutzfeldt-Jakob disease patients",
abstract = "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.",
author = "Judith L{\"o}ffler and Susanne Krasemann and Inga Zerr and Jakob Matschke and Markus Glatzel",
year = "2014",
month = jan,
day = "1",
language = "English",
volume = "3",
pages = "152--7",
journal = "Am J Neurodegener Dis",
issn = "2165-591X",
publisher = "e-Century Publishing Corporation",
number = "3",

}

RIS

TY - JOUR

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 -