scholarly journals SARM Is Required for Neuronal Injury and Cytokine Production in Response to Central Nervous System Viral Infection

2013 ◽  
Vol 191 (2) ◽  
pp. 875-883 ◽  
Author(s):  
Ying-Ju Hou ◽  
Rebecca Banerjee ◽  
Bobby Thomas ◽  
Carl Nathan ◽  
Adolfo García-Sastre ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Viral Infection ◽  
Cytokine Production ◽  
Neuronal Injury

MENINGOENCEPHALITIS AND LABORATORY EVIDENCE OF TRIPLE INFECTION WITH CALIFORNIA ENCEPHALITIS VIRUS, ECHOVIRUS II, AND MUMPS

PEDIATRICS ◽  
1973 ◽  
Vol 51 (4) ◽  
pp. 680-684 ◽  
Author(s):  
Henry H. Balfour ◽  
Gregory L. Seifert ◽  
Milton H. Seifert ◽  
Paul G. Quie ◽  
Charlene K. Edelman ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Viral Infection ◽  
Central Nervous System Disease ◽  
Encephalitis Virus ◽  
Laboratory Findings ◽  
Laboratory Evidence ◽  
System Disease ◽  
Triple Infection ◽  
Echovirus Type

This report emphasizes that in acute central nervous system disease, multiple viral agents may be implicated in the same patient. A 6-year-old girl with meningoencephalitis had laboratory evidence for simultaneous or closely spaced infections with California encephalitis virus, echovirus type 11, and mumps. Documentation of the finding of triple viral infection was based on at least two laboratory findings for each agent. The patient lived in an area where California encephalitis was prevalent.

scholarly journals Seizures and epilepsy secondary to viral infection in the central nervous system

2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Peng Zhang ◽  
Yuting Yang ◽  
Jialin Zou ◽  
Xinrui Yang ◽  
Qiankun Liu ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Viral Infection ◽  
The Central Nervous System

Detection by Hybridization of Viral Infection of the Human Central Nervous System

1984 ◽  
Vol 436 (1 Multiple Scle) ◽  
pp. 103-108 ◽  
Author(s):  
ASHLEY T. HAASE ◽  
LINDA STOWRING ◽  
PETER VENTURA ◽  
JACK BURKS ◽  
GEORGE EBERS ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Viral Infection ◽  
Human Central Nervous System

scholarly journals Differential Regulation of Interferon Regulatory Factor (IRF)-7 and IRF-9 Gene Expression in the Central Nervous System during Viral Infection

2005 ◽  
Vol 79 (12) ◽  
pp. 7514-7527 ◽  
Author(s):  
Shalina S. Ousman ◽  
Jianping Wang ◽  
Iain L. Campbell
Keyword(s):  
Gene Expression ◽  
Central Nervous System ◽  
Nervous System ◽  
Viral Infection ◽  
Mononuclear Cells ◽  
Lymphocytic Choriomeningitis ◽  
The Central Nervous System ◽  
Ifn Γ ◽  
The Brain ◽  
Lcmv Infection

ABSTRACT Interferon regulatory factors (IRFs) are a family of transcription factors involved in the regulation of the interferons (IFNs) and other genes that may have an essential role in antiviral defense in the central nervous system, although this is currently not well defined. Therefore, we examined the regulation of IRF gene expression in the brain during viral infection. Several IRF genes (IRF-2, -3, -5, -7, and -9) were expressed at low levels in the brain of uninfected mice. Following intracranial infection with lymphocytic choriomeningitis virus (LCMV), expression of the IRF-7 and IRF-9 genes increased significantly by day 2. IRF-7 and IRF-9 gene expression in the brain was widespread at sites of LCMV infection, with the highest levels in infiltrating mononuclear cells, microglia/macrophages, and neurons. IRF-7 and IRF-9 gene expression was increased in LCMV-infected brain from IFN-γ knockout (KO) but not IFN-α/βR KO animals. In the brain, spleen, and liver or cultured glial and spleen cells, IRF-7 but not IRF-9 gene expression increased with delayed kinetics in the absence of STAT1 but not STAT2 following LCMV infection or IFN-α treatment, respectively. The stimulation of IRF-7 gene expression by IFN-α in glial cell culture was prevented by cycloheximide. Thus, (i) many of the IRF genes were expressed constitutively in the mouse brain; (ii) the IRF-7 and IRF-9 genes were upregulated during viral infection, a process dependent on IFN-α/β but not IFN-γ; and (iii) IRF-7 but not IRF-9 gene expression can be stimulated in a STAT1-independent but STAT2-dependent fashion via unidentified indirect pathways coupled to the activation of the IFN-α/β receptor.

Sign in / Sign up

Export Citation Format

Share Document