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Updated: Apr 28, 2026
Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
Published on: June 22, 2016
Cell entry of lymphocytic choriomeningitis virus is restricted in myotubes
Masaharu Iwasaki1, Shuzo Urata1, Yoshitake Cho2
1Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA, USA.
Abstract:
In mice persistently infected since birth with the prototypic arenavirus lymphocytic choriomeningitis viurs, viral antigen and RNA are readily detected in most organs and cell types but remarkably absent in skeletal muscle. Here we report that mouse C2C12 myoblasts that are readily infected by LCMV, become highly refractory to LCMV infection upon their differentiation into myotubes. Myotube's resistance to LCMV was not due to an intracellular restriction of virus replication but rather an impaired cell entry mediated by the LCMV surface glycoprotein. Our findings provide an explanation for the observation that in LCMV carrier mice myotubes, which are constantly exposed to blood-containing virus, remain free of viral antigen and RNA despite myotubes express high levels of the LCMV receptor alpha dystroglycan and do not pose an intracellular blockade to LCMV multiplication.
Insights
Skeletal muscle cells resist lymphocytic choriomeningitis virus (LCMV) infection after differentiation. This resistance is due to impaired viral entry, not intracellular factors, explaining LCMV absence in carrier mice.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Persistent lymphocytic choriomeningitis virus (LCMV) infection in mice typically shows viral presence in most organs.
- Skeletal muscle, however, remarkably lacks detectable viral antigen and RNA in LCMV-carrier mice.
Purpose of the Study:
- To investigate the mechanism behind the absence of LCMV in skeletal muscle of persistently infected mice.
- To determine why differentiated muscle cells (myotubes) are resistant to LCMV infection.
Main Methods:
- Infection of mouse C2C12 myoblasts and differentiated myotubes with LCMV.
- Analysis of viral replication and entry.
- Assessment of LCMV receptor (alpha-dystroglycan) expression.
Main Results:
- Differentiated C2C12 myotubes become highly refractory to LCMV infection compared to myoblasts.
- Myotube resistance is mediated by impaired viral entry, specifically involving the LCMV surface glycoprotein.
- This resistance occurs despite high expression of the LCMV receptor, alpha-dystroglycan, on myotubes.
Conclusions:
- LCMV entry into differentiated skeletal muscle cells is significantly restricted.
- Impaired viral entry, not intracellular replication blockade, explains LCMV absence in mouse skeletal muscle.
- Findings elucidate a key aspect of viral persistence and tissue tropism in arenavirus infections.
