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Irreversible splenic atrophy following chronic LCMV infection is associated with compromised immunity in mice
Achire N Mbanwi1, Chao Wang1, Kaoru Geddes1
1Department of Immunology, University of Toronto, Toronto, ON, Canada.
Abstract:
Lymphocytic choriomeningitis virus clone 13 (LCMV13) infection of mice is a widely used model for investigating the mechanisms driving persistent viral infection in humans. LCMV13 disrupts splenic architecture early during infection, but this returns to normal within a few weeks. However, the long-term effects of LCMV13 infection on splenic structure have not been reported. Here, we report that persistent infection with LCMV13 results in sustained splenic atrophy that persists for at least 500 days following infection, whereas infection with the acutely infecting LCMV Armstrong is associated with a return to preinfection spleen weights. Splenic atrophy is associated with loss of T, B, and non-B non-T cells, with B cells most significantly affected. These effects were partly ameliorated by anti-NK1.1 or anti-CD8 antibody treatment. Antigen presentation was detectable at the time of contraction of the spleen, but no longer detected at late time points, suggesting that continued antigen presentation is not required to maintain splenic atrophy. Immunity to Salmonella infection and influenza vaccination were decreased after the virus was no longer detected. Thus splenic atrophy following LCMV13 infection is irreversible and may contribute to impaired immunity following clearance of LCMV13.
Insights
Persistent lymphocytic choriomeningitis virus clone 13 (LCMV13) infection causes long-lasting splenic atrophy in mice, impacting immune cell populations. This sustained spleen damage may lead to impaired immunity even after viral clearance.
Area of Science:
- Virology
- Immunology
- Pathology
Background:
- Lymphocytic choriomeningitis virus clone 13 (LCMV13) is a model for persistent viral infections.
- LCMV13 causes early splenic architecture disruption, but long-term effects are unknown.
- Acute LCMV Armstrong infection allows spleen structure recovery.
Purpose of the Study:
- To investigate the long-term effects of LCMV13 infection on spleen structure and cellular composition.
- To determine if splenic atrophy is reversible and its relationship with antigen presentation.
- To assess the impact of LCMV13-induced splenic atrophy on adaptive immunity.
Main Methods:
- Infection of mice with LCMV13 and LCMV Armstrong.
- Monitoring spleen weight and cellularity over 500 days.
- Flow cytometry to analyze T, B, and NK cell populations.
- Antibody treatment (anti-NK1.1, anti-CD8) to assess amelioration.
- Assessment of antigen presentation and immune responses to Salmonella and influenza.
Main Results:
- Persistent LCMV13 infection led to sustained splenic atrophy for at least 500 days.
- Splenic atrophy involved significant loss of T, B, and non-B non-T cells, particularly B cells.
- Anti-NK1.1 or anti-CD8 treatment partially ameliorated atrophy.
- Antigen presentation was transient, not required for maintaining atrophy.
- Impaired immunity to Salmonella infection and influenza vaccination was observed post-viral clearance.
Conclusions:
- LCMV13-induced splenic atrophy is a persistent and potentially irreversible condition.
- The atrophy is associated with significant immune cell loss and impaired adaptive immunity.
- Splenic atrophy may contribute to long-term immune dysfunction following LCMV13 infection.
