Literature DB >> 28187911

What Kaplan-Meier survival curves don't tell us about CNS disease.

Katelyn D Miller1, Glenn F Rall2.   

Abstract

Central nervous system consequences of viral infections are rare, but when they do occur, they are often serious and clinically challenging to manage. Our awareness of the perils of neuroinvasion by viruses is growing: the recently appreciated impact of Ebola and Zika virus infections on CNS integrity, decreases in vaccination coverage for potentially neurotropic viruses such as measles, and increased neurovirulence of some influenza strains collectively highlight the need for a better understanding of the viral-neural interaction. Defining these interactions and how they result in neuropathogenesis is paramount for the development of better clinical strategies, especially given the limited treatment options that are available due to the unique physiology of the brain that limits migration of blood-borne molecules into the CNS parenchyma. In this perspective, we discuss some unique aspects of neuronal viral infections and immune-mediated control that impact the pathogenic outcomes of these infections. Further, we draw attention to an often overlooked aspect of neuropathogenesis research: that lack of overt disease, which is often equated with survival post-infection, likely only scratches the surface of the myriad ways by which neurotropic infections can impair CNS function.
Copyright © 2017 Elsevier B.V. All rights reserved.

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Year:  2017        PMID: 28187911      PMCID: PMC5474346          DOI: 10.1016/j.jneuroim.2017.01.020

Source DB:  PubMed          Journal:  J Neuroimmunol        ISSN: 0165-5728            Impact factor:   3.478


  50 in total

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2.  Neuronal cells are deficient in loading peptides onto MHC class I molecules.

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3.  Detailed in vivo analysis of interferon-gamma induced major histocompatibility complex expression in the the central nervous system: astrocytes fail to express major histocompatibility complex class I and II molecules.

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4.  RAG-2-deficient mice lack mature lymphocytes owing to inability to initiate V(D)J rearrangement.

Authors:  Y Shinkai; G Rathbun; K P Lam; E M Oltz; V Stewart; M Mendelsohn; J Charron; M Datta; F Young; A M Stall
Journal:  Cell       Date:  1992-03-06       Impact factor: 41.582

5.  Persistence of viral RNA in mouse brains after recovery from acute alphavirus encephalitis.

Authors:  B Levine; D E Griffin
Journal:  J Virol       Date:  1992-11       Impact factor: 5.103

6.  Contralesional motor deficits after unilateral stroke reflect hemisphere-specific control mechanisms.

Authors:  Saandeep Mani; Pratik K Mutha; Andrzej Przybyla; Kathleen Y Haaland; David C Good; Robert L Sainburg
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7.  Type I interferons are essential in controlling neurotropic coronavirus infection irrespective of functional CD8 T cells.

Authors:  Derek D C Ireland; Stephen A Stohlman; David R Hinton; Roscoe Atkinson; Cornelia C Bergmann
Journal:  J Virol       Date:  2007-10-10       Impact factor: 5.103

8.  Human membrane cofactor protein (CD46) acts as a cellular receptor for measles virus.

Authors:  D Naniche; G Varior-Krishnan; F Cervoni; T F Wild; B Rossi; C Rabourdin-Combe; D Gerlier
Journal:  J Virol       Date:  1993-10       Impact factor: 5.103

9.  Neuronal Interferon Signaling Is Required for Protection against Herpes Simplex Virus Replication and Pathogenesis.

Authors:  Pamela C Rosato; David A Leib
Journal:  PLoS Pathog       Date:  2015-07-08       Impact factor: 6.823

10.  A Mouse Model of Chronic West Nile Virus Disease.

Authors:  Jessica B Graham; Jessica L Swarts; Courtney Wilkins; Sunil Thomas; Richard Green; Aimee Sekine; Kathleen M Voss; Renee C Ireton; Michael Mooney; Gabrielle Choonoo; Darla R Miller; Piper M Treuting; Fernando Pardo Manuel de Villena; Martin T Ferris; Shannon McWeeney; Michael Gale; Jennifer M Lund
Journal:  PLoS Pathog       Date:  2016-11-02       Impact factor: 6.823

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