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Published on: November 9, 2019
Restricted Theiler's murine encephalomyelitis virus infection in murine macrophages induces apoptosis
Abstract:
Increasing evidence suggests that macrophages (M(phi)s) are necessary for persistence of Theiler's murine encephalomyelitis virus (TMEV) in the mouse central nervous system. Analysis of BeAn virus infection in the Mphi cell lines P388D1, J774A.1 and PU5-1.8, which are intermediate in their state of differentiation and resemble multifunctional resident M(phi)s, revealed restricted TMEV growth. As a result of the restricted infection, these Mphi cell lines were induced to undergo apoptosis as demonstrated by cellular morphology, DNA fragmentation, caspase protease activity, and in individual cells, by terminal deoxytransferase dUTP nick-end labelling (TUNEL).
Insights
Macrophages are crucial for Theiler's murine encephalomyelitis virus persistence. Restricted virus growth in these cells triggered apoptosis, indicating a novel cell death pathway during viral infection.
Area of Science:
- Neurovirology
- Immunology
- Cell Biology
Background:
- Macrophages (M(phi)s) play a key role in the central nervous system's response to viral infections.
- Theiler's murine encephalomyelitis virus (TMEV) persistence in the mouse CNS is increasingly linked to macrophage activity.
Purpose of the Study:
- To investigate the interaction between TMEV and macrophage cell lines.
- To determine the effect of restricted TMEV infection on macrophage viability and function.
Main Methods:
- Infection of macrophage cell lines (P388D1, J774A.1, PU5-1.8) with BeAn virus (a strain of TMEV).
- Analysis of viral growth kinetics within these cell lines.
- Assessment of apoptosis using morphological examination, DNA fragmentation assays, caspase activity measurement, and TUNEL staining.
Main Results:
- Macrophage cell lines exhibited restricted growth of TMEV.
- This restricted infection induced apoptosis in the infected macrophages.
- Apoptosis was confirmed through multiple indicators including DNA fragmentation and caspase activation.
Conclusions:
- Macrophages are implicated in the persistence of TMEV within the CNS.
- Restricted TMEV infection of macrophages leads to programmed cell death (apoptosis).
- This study reveals a potential mechanism of macrophage-mediated viral clearance or regulation via apoptosis.
