scholarly journals INTRAPERITONEAL AND INTRACEREBRAL ROUTES IN SERUM PROTECTION TESTS WITH THE VIRUS OF EQUINE ENCEPHALOMYELITIS

1938 ◽  
Vol 68 (5) ◽  
pp. 761-777 ◽  
Author(s):  
Peter K. Olitsky ◽  
Carl G. Harford

Minute amounts of antiserum injected intraperitoneally protect against large doses of equine encephalomyelitis virus given intramuscularly or intraperitoneally in 12 to 15 day old mice. Antiserum given intraperitoneally with virus intracerebrally or intranasally results in little or no protection. These phenomena occur as well when serum-virus mixtures are injected at the different sites. The marked variation of the protective capacity of antiserum as thus displayed would appear to be dependent upon the differing pathways of progression of the virus from the site of injection to the central nervous system.

1992 ◽  
Vol 591 (2) ◽  
pp. 248-252 ◽  
Author(s):  
Raffaello Nemni ◽  
Sandro Iannaccone ◽  
Angelo Quattrini ◽  
Salvatore Smirne ◽  
Maria Sessa ◽  
...  

2002 ◽  
Vol 76 (24) ◽  
pp. 13049-13054 ◽  
Author(s):  
Kunihiko Asakura ◽  
Harunobu Murayama ◽  
Toshiki Himeda ◽  
Yoshiro Ohara

ABSTRACT TO subgroup strains of Theiler's murine encephalomyelitis virus (TMEV) synthesize L* protein from an alternative initiation codon. We first demonstrated L* expression in the central nervous system (CNS) of TMEV-infected mice during the acute phase of infection by immunoprecipitation and immunoblotting with anti-L* antibody. In addition, we generated mutant viruses which synthesize FLAG or 3xFLAG epitope-tagged L* protein. With a mutant virus expressing 3xFLAG epitope-tagged L*, designated DA/3xFLAGL*, we investigated L* in the CNS in the acute phase of infection. DA/3xFLAGL* did not change the virus tropism in comparison with wild-type virus, and L* was clearly identified in the CNS in both susceptible and resistant strains of mice. Double immunolabeling studies showed that L* is colocalized with TMEV polyprotein and exclusively expressed in neurons.


1999 ◽  
Vol 73 (2) ◽  
pp. 1637-1639 ◽  
Author(s):  
John J. Bright ◽  
Moses Rodriguez ◽  
Subramaniam Sriram

ABSTRACT Experimental allergic encephalomyelitis (EAE) and Theiler’s murine encephalomyelitis virus (TMEV) disease are two demyelinating diseases of the central nervous system (CNS) that serve as animal models for multiple sclerosis. Th1 cells are thought to play a role in the pathogenesis of CNS demyelination in both these diseases. We show here the differential influence of interleukin 12, a critical cytokine for the development of Th1 cells in EAE and TMEV disease.


2012 ◽  
Vol 3 (3) ◽  
Author(s):  
Amanda Brown

AbstractOsteopontin (OPN) is a pro-inflammatory cytokine that can be secreted from many cells including activated macrophages and T-lymphocytes. Elevated levels of osteopontin in the plasma, cerebrospinal fluid or brain of individuals with neurodegenerative diseases such as multiple sclerosis (MS), Parkinson’s and Alzheimer’s disease and more recently in HIV-associated neurocognitive disorder has been reported. However, except for the case of MS, little is known regarding the molecular mechanisms by which OPN may exacerbate disease. Alternatively, OPN through its ability to promote cell survival may in some contexts function in the brain in a protective capacity. OPN has several protein motifs that allow it to engage with several different signaling pathways involved in immunity and inflammation. A better understanding of the cellular pathways that are regulated by OPN in cells of the central nervous system is required to uncover its putative role in neuronal homeostasis.


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