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Measles infection of the central nervous system
Jürgen Schneider-Schaulies1, Volker ter Meulen, Sibylle Schneider-Schaulies
1Institute for Virology and Immunobiology, University of Würzburg, Würzburg, Germany. jss@vim.uni-wuerzburg.de
Abstract:
Central nervous system (CNS) complications occurring early and late after acute measles are serious and often fatal. In spite of functional cell-mediated immunity and high antiviral antibody titers, an immunological control of the CNS infection is not achieved in patients suffering from subacute sclerosing panencephalitis (SSPE). The known cellular receptors for measle virus (MV) in humans, CD46 and CD150 (signaling lymphocyte activation molecule, SLAM), are important components of the viral tropism by mediating binding and entry to peripheral cells. Because neural cells do not express SLAM and only sporadically CD46, virus entry to neural cells, and spread within the CNS, remain mechanistically unclear. Mice, hamsters, and rats have been used as model systems to study MV-induced CNS infections, and revealed interesting aspects of virulence, persistence, the immune response, and prerequisites of protection. With the help of recombinant MV and mice expressing transgenic receptors, questions such as receptor-dependent viral spread, or viral determinants of virulence, have been investigated. However, many questions concerning the human MV-induced CNS diseases are still open.
Insights
Measles virus (MV) causes severe central nervous system (CNS) diseases like subacute sclerosing panencephalitis (SSPE). Understanding MV entry into neural cells is crucial for developing effective treatments and preventing fatal outcomes.
Area of Science:
- Virology
- Neuroscience
- Immunology
Background:
- Measles virus (MV) can cause severe, often fatal, central nervous system (CNS) complications, including subacute sclerosing panencephalitis (SSPE).
- Despite robust immune responses, immunological control of CNS infections by MV is often insufficient in SSPE patients.
- The precise mechanisms of MV entry and spread within the CNS remain unclear, as neural cells lack typical MV receptors (CD46, SLAM).
Purpose of the Study:
- To investigate the mechanisms of measles virus (MV) entry and spread within the central nervous system (CNS).
- To understand the viral determinants of virulence and receptor-dependent spread in MV-induced CNS diseases.
- To explore potential therapeutic strategies by clarifying MV neurotropism.
Main Methods:
- Utilized animal models (mice, hamsters, rats) to study MV-induced CNS infections.
- Employed recombinant MV strains and transgenic mice expressing specific receptors.
- Investigated viral tropism, persistence, immune response, and protection prerequisites.
Main Results:
- Animal models provided insights into MV virulence, persistence, and immune responses in the CNS.
- Recombinant MV and transgenic models facilitated studies on receptor-dependent viral spread.
- Key questions regarding MV neurotropism and determinants of CNS disease remain under investigation.
Conclusions:
- Current understanding of MV entry into neural cells and CNS spread is incomplete.
- Animal models are valuable tools for studying MV-induced CNS pathology.
- Further research is needed to elucidate the mechanisms underlying human MV-induced CNS diseases.