scholarly journals microRNA-219 Reduces Viral Load and Pathologic Changes in Theiler's Virus-Induced Demyelinating Disease

2018 ◽  
Vol 26 (3) ◽  
pp. 730-743 ◽  
Author(s):  
Ana Lis Moyano ◽  
Jeffrey Steplowski ◽  
Haibo Wang ◽  
Kyung-No Son ◽  
Diana I. Rapolti ◽  
...  
1999 ◽  
Vol 73 (10) ◽  
pp. 7965-7971 ◽  
Author(s):  
Stéphanie Aubagnac ◽  
Michel Brahic ◽  
Jean-François Bureau

ABSTRACT Theiler’s virus causes a persistent infection and a demyelinating disease of mice which is a model for multiple sclerosis. Susceptibility to viral persistence maps to several loci, including the interferon gamma locus. Inactivating the gene coding for the interferon gamma receptor makes 129/Sv mice susceptible to persistent infection and clinical disease, whereas inactivating the interferon gamma gene makes C57BL/6 mice susceptible to persistent infection but not to clinical disease. This difference in phenotype is due to the difference in genetic background. Clinical disease depends on high viral load andTmevd5, a locus on chromosome 11. These results have consequences for the identification of viruses which might be implicated in multiple sclerosis.


Genetics ◽  
1998 ◽  
Vol 148 (4) ◽  
pp. 1941-1949
Author(s):  
J-F Bureau ◽  
K M Drescher ◽  
L R Pease ◽  
T Vikoren ◽  
M Delcroix ◽  
...  

Abstract Theiler's murine encephalomyelitis virus causes a chronic demyelinating disease in susceptible strains of mice that is similar to human multiple sclerosis. Several nonmajor histocompatibility complex–linked genes have been implicated as determinants of susceptibility or resistance to either demyelination or virus persistence. In this study, we used linkage analysis of major histocompatibility complex identical H-2d (DBA/2J × B10.D2) F2 intercross mice to identify loci associated with susceptibility to virus-induced demyelinating disease. In a 20-cM region on chromosome 14, we identified four markers, D14Mit54, D14Mit60, D14Mit61, and D14Mit90 that are significantly associated with demyelination. Because two peaks were identified, one near D14Mit54 and one near D14Mit90, it is possible that two loci in this region are involved in controlling demyelination.


1994 ◽  
Vol 55 (2) ◽  
pp. 143-152 ◽  
Author(s):  
L PULLEN ◽  
S MILLER ◽  
M DALCANTO ◽  
P VANDERMEIDE ◽  
B KIM

2016 ◽  
Vol 2016 ◽  
pp. 1-4 ◽  
Author(s):  
T. Nanda

Progressive multifocal leukoencephalopathy (PML) is a rare demyelinating disease most common in immunodeficient patients. It occurs due to reactivation of the John Cunningham Virus (JCV) and carries a poor prognosis, with a median life expectancy of 6 months. We report a case of a 66-year-old man with a history of HCV related cirrhosis (HCV) and hepatocellular carcinoma (HCC) who was found to have PML in the setting of a negative viral load in the CSF and a CD4+ >200. He initially presented with two weeks of mild confusion and word-finding difficulty concerning for hepatic encephalopathy. An MRI was notable for extensive T2/FLAIR hyperintensity signal in the left temporal lobe. Brain biopsy was positive for JCV. PML is rare in immunocompetent individuals, especially in the setting of a negative viral load. It is possible, however, that transient states of immunosuppression may have been responsible in this case. Although viral load was reported as negative, virus may still have been detected but was below the quantifiable threshold. It is important for clinicians to note that a negative result does not necessarily exclude the possibility of PML, and care should be taken to review lab values on viral load in closer detail.


Sign in / Sign up

Export Citation Format

Share Document