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11:28
Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
Published on: October 7, 2011
Measles virus interactions with cellular receptors: consequences for viral pathogenesis
J Schneider-Schaulies1, V ter Meulen, S Schneider-Schaulies
1Institute for Virology and Immunobiology, University of Würzburg, Würzburg, Germany. jss@vim.uni-wuerzburg.de
Journal of Neurovirology
|October 3, 2001
Summary
Measles virus (MV) interactions with cellular receptors, including CD46 and CD150, drive viral pathogenesis. Understanding these interactions is key to addressing measles-related global health issues.
Area of Science:
- Virology
- Immunology
- Neuroscience
Background:
- Measles virus (MV) causes severe complications, including fatal central nervous system (CNS) issues.
- Transient immunosuppression post-measles is a primary driver of global morbidity and mortality.
- MV pathogenesis involves interactions with cellular receptors on neural and lymphoid cells.
Purpose of the Study:
- To review the interactions between measles virus and cellular receptors.
- To elucidate the role of these interactions in viral pathogenesis.
- To highlight the significance of MV receptor interactions in measles-related health outcomes.
Main Methods:
- Review of existing literature on measles virus-host interactions.
- Analysis of the roles of known MV receptors (CD46, CD150).
- Exploration of potential signaling pathways modulated by MV glycoproteins.
Main Results:
- CD46 and CD150 are cognate receptors mediating MV binding and entry, crucial for viral tropism.
- Unknown cellular surface molecules may interact with MV glycoproteins, independent of viral uptake.
- These interactions can modulate cellular functions, including survival and proliferation.
Conclusions:
- MV receptor interactions are central to its pathogenesis.
- Beyond entry, MV glycoproteins can trigger signaling pathways affecting host cells.
- Further research into these molecular interactions is vital for understanding and combating measles.
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