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Measles virus: immunomodulation and cell tropism as pathogenicity determinants
Sibylle Schneider-Schaulies1, Jürgen Schneider-Schaulies, Stefan Niewiesk
1Institute for Virology and Immunobiology, University of Würzburg, Versbacher Str. 7, Germany. s-s-s@vim.uni-wuerzburg.de
Abstract:
As important determinants of measles virus (MV) pathogenicity, the MV glycoproteins play a key role in conferring the cellular tropism of this virus, but also in modulating the activity of immunocompetent cells. Whereas all MV strains are able to use CD150 (SLAM) for binding and entry into target cells, only certain, mainly vaccine, strains, can use both CD46 and CD150. Both molecules are down-regulated from the cell surface and this is brought about by both infection and contact with the MV H protein of strains that are able to interact with these molecules. Whereas down-regulation of CD46 could be linked to enhanced sensitivity to complement-mediated lysis, and may thus represent an attenuation marker for vaccine strains, pathogenetic consequences of CD150 down-regulation are unknown as yet. Although the role of CD150 is not entirely clear, viruses containing a wild-type strain-derived H protein revealed a particular tropism for human dendritic cells in vitro, and replicated well in secondary lymphatic tissues of cotton rats where they were also able to cause immunosuppression, as documented by an impaired proliferative response of lymphocytes ex vivo. Most likely, inhibition of T cell expansion by these cells is brought about by another activity of the MV glycoprotein complex, namely by disrupting a pathway important for S-phase entry of T cells, by a mere surface contact.
Insights
Measles virus (MV) glycoproteins bind to CD150 and CD46, down-regulating them on cell surfaces. Wild-type MV strains with specific H proteins cause immunosuppression by impairing T cell expansion.
Area of Science:
- Virology
- Immunology
Background:
- Measles virus (MV) glycoproteins determine pathogenicity and cellular tropism.
- MV utilizes CD150 (SLAM) for entry; some strains also use CD46.
- Both CD150 and CD46 are down-regulated upon MV infection or H protein interaction.
Purpose of the Study:
- To investigate the role of MV glycoproteins in cellular tropism and immune modulation.
- To understand the consequences of CD46 and CD150 down-regulation by MV.
- To explore the mechanisms of MV-induced immunosuppression.
Main Methods:
- In vitro tropism studies using MV strains and target cells expressing CD150 and/or CD46.
- Analysis of CD46 and CD150 cell surface expression following MV infection or H protein exposure.
- Ex vivo assessment of lymphocyte proliferation in response to MV infection in animal models.
- Investigation of T cell activation pathways affected by MV glycoproteins.
Main Results:
- All MV strains bind CD150; certain strains (mainly vaccine) bind both CD150 and CD46.
- MV infection and H protein interaction lead to CD150 and CD46 down-regulation.
- CD46 down-regulation may enhance sensitivity to complement lysis, potentially an attenuation marker.
- Wild-type MV strains show tropism for dendritic cells and cause immunosuppression in cotton rats.
- Impaired lymphocyte proliferation ex vivo suggests MV inhibits T cell expansion.
Conclusions:
- MV glycoproteins play a critical role in viral pathogenicity and immune evasion.
- Down-regulation of CD46 and CD150 are key mechanisms employed by MV.
- Wild-type MV H protein interaction with immune cells, particularly dendritic cells, leads to immunosuppression.
- MV may inhibit T cell proliferation by disrupting S-phase entry pathways via surface contact.
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