José Antonio Gómez
Graduate Student (Microbiology and Immunology)

B.S. Chemical Biology, University of California - Berkeley, 2006.
D321 Fairchild
299 Campus Drive
Stanford CA 94305-5124
Research Summary

The infection of mice with Theiler’s Murine Encephalomyelitis Virus (Theiler’s virus) is a model system to study the effects of persistent infection in the central nervous system (CNS). Theiler’s virus induces a biphasic CNS disease in susceptible mice that begins with an acute encephalomyelitis. Mouse strains resistant to persistence clear the viral infection within 14 days, whereas mice that are susceptible develop a chronic infection that results in development focal demyelinated lesions, which are reminiscent of multiple sclerosis in humans (Clinical Micro. Rev. 2004, 17:174-207).

Genetic loci that confer differences between susceptibility between B10.S and SJL/J mice have been mapped (Genetics 1999, 152: 385-92). One of these loci, Tmevp3, is located on chromosome 10 and affects viral loads in the late phase of infection. Tmevp3 has been finely mapped to about 500kb and contains four genes including a non-coding RNA, Tmevpg1. Tmevpg1 is expressed most abundantly in the spleen and thymus. Tmevpg1 RNA is expressed in resting CD4+ and CD8+ T-cells,but its abundance falls sharply upon T-cell stimulation. Its abundance is inversely proportional to that of IFN-gamma mRNA, which quickly accumulates upon stimulation (J. of Virology 2003, 77:5632-5638).

To test the hypothesize that Tmevpg1 RNA is involved in the regulation of IFN-gamma mRNA expression, we are testing the effect of overexpressing Tmevpg1 RNA in T-cells on IFNG-gamma expression. To test for allele-specific differences in Tmevpg1 overexpression, we are introducing both the SJL/J and B10.s Tmevpg1 cDNA into primary T-cells from both SJL/J and B10.S mice.
Copyright 2006 - 2010. The Laboratory of Karla Kirkegaard, Ph.D. All rights reserved.