TY - JOUR
T1 - Injection of the sciatic nerve with TMEV
T2 - A new model for peripheral nerve demyelination
AU - Drescher, Kristen M.
AU - Tracy, Steven M.
N1 - Funding Information:
This work was supported in part by grants from the NIH (1 P20 RR018788-01) (KMD), the Nebraska Tobacco Settlement, LB 692 (KMD), the Juvenile Diabetes Research Foundation (ST), and the American Diabetes Association (ST). This investigation was conducted in a facility constructed with support from Research Facilities Improvement Program (1 C06 RR17417-01) from the National Center for Research Resources, National Institutes of Health.
PY - 2007/3/1
Y1 - 2007/3/1
N2 - Demyelination of the human peripheral nervous system (PNS) can be caused by diverse mechanisms including viral infection. Despite association of several viruses with the development of peripheral demyelination, animal models of the condition have been limited to disease that is either autoimmune or genetic in origin. We describe here a model of PNS demyelination based on direct injection of sciatic nerves of mice with the cardiovirus, Theiler's murine encephalomyelitis virus (TMEV). Sciatic nerves of FVB mice develop inflammatory cell infiltration following TMEV injection. Schwann cells and macrophages are infected with TMEV. Viral replication is observed initially in the sciatic nerves and subsequently the spinal cord. Sciatic nerves are demyelinated by day 5 post-inoculation (p.i.). Injecting sciatic nerves of scid mice resulted in increased levels of virus recovered from the sciatic nerve and spinal cord relative to FVB mice. Demyelination also occurred in scid mice and by 12 days p.i., hindlimbs were paralyzed. This new model of virus-induced peripheral demyelination may be used to dissect processes involved in protection of the PNS from viral insult and to study the early phases of lesion development.
AB - Demyelination of the human peripheral nervous system (PNS) can be caused by diverse mechanisms including viral infection. Despite association of several viruses with the development of peripheral demyelination, animal models of the condition have been limited to disease that is either autoimmune or genetic in origin. We describe here a model of PNS demyelination based on direct injection of sciatic nerves of mice with the cardiovirus, Theiler's murine encephalomyelitis virus (TMEV). Sciatic nerves of FVB mice develop inflammatory cell infiltration following TMEV injection. Schwann cells and macrophages are infected with TMEV. Viral replication is observed initially in the sciatic nerves and subsequently the spinal cord. Sciatic nerves are demyelinated by day 5 post-inoculation (p.i.). Injecting sciatic nerves of scid mice resulted in increased levels of virus recovered from the sciatic nerve and spinal cord relative to FVB mice. Demyelination also occurred in scid mice and by 12 days p.i., hindlimbs were paralyzed. This new model of virus-induced peripheral demyelination may be used to dissect processes involved in protection of the PNS from viral insult and to study the early phases of lesion development.
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U2 - 10.1016/j.virol.2006.09.009
DO - 10.1016/j.virol.2006.09.009
M3 - Article
C2 - 17028060
AN - SCOPUS:33846857968
VL - 359
SP - 233
EP - 242
JO - Virology
JF - Virology
SN - 0042-6822
IS - 1
ER -