Key result
Active TMEV replication with high viral genome loads in the spinal cord is required to drive increased Th1 cytokine expression and subsequent chronic demyelinating disease in susceptible mice.
Population
6-week-old female SJL/J, SJL/H, and B6 mice
Comparison
Inoculation in the right cerebral hemisphere… vs Resistant B6 mice and uninfected control tissues
Design
Preclinical
Follow-up
Up to 145 days post-infection
Authors
Loading...
Hypothesis-generating in TMEV mouse model; leaves open whether active replication drives human demyelinating disease.
TMEV persistence and subsequent demyelinating disease in susceptible mice require active viral replication that drives pro-inflammatory Th1 cytokine expression.
Trottier et al. (2004) studied Theiler's murine encephalomyelitis virus (TMEV) infection. Theiler's murine encephalomyelitis virus (BeAn strain) vs. Resistant B6 mice was evaluated on Viral RNA copy equivalents and pro-inflammatory cytokine mRNA expression. Active TMEV replication with high viral genome loads in the spinal cord is required to drive increased Th1 cytokine expression and subsequent chronic demyelinating disease in susceptible mice.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: