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Published on: August 25, 2013
The role of sphingomyelin breakdown in measles virus immunmodulation
Elita Avota1, Sibylle Schneider-Schaulies
1Institute for Virology and Immunobiology, University of Wuerzburg, Wuerzburg, Germany.
Abstract:
Measles virus (MV) efficiently causes generalized immunosuppression which accounts to a major extent for cases of measles-asscociated severe morbidity and mortality. MV infections alter many functions of antigen presenting cells (APC) (dendritic cells (DCs)) and lymphocytes, yet many molecular targets of the virus remain poorly defined. Cellular interactions and effector functions of DCs and lymphocytes are regulated by surface receptors. Associating with other proteins involved in cell signaling, receptors form part of receptosomes that respond to and transmit external signals through dynamic interctions with the cytoskeleton. Alterations in the composition and metabolism of membrane sphingolipids have a substantial impact on both processes. In this review we focus on the regulation of sphingomyelinase activity and ceramide release in cells exposed to MV and discuss the immunosuppressive role of sphingomyelin breakdown induced by MV.
Insights
Measles virus (MV) infection suppresses the immune system by altering sphingolipid metabolism. This breakdown of sphingomyelin and subsequent ceramide release contributes to measles-associated morbidity and mortality.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Measles virus (MV) causes significant immunosuppression, leading to severe illness and death.
- MV affects antigen-presenting cells (APCs) like dendritic cells (DCs) and lymphocytes, but molecular targets are unclear.
- Cellular functions rely on surface receptors and their interactions with signaling proteins and the cytoskeleton.
Purpose of the Study:
- To review the regulation of sphingomyelinase activity and ceramide release in cells infected with MV.
- To discuss the immunosuppressive role of sphingomyelin breakdown during MV infection.
Main Methods:
- Literature review focusing on sphingolipid metabolism and MV infection.
- Analysis of cellular signaling pathways involving receptors and the cytoskeleton.
- Examination of ceramide release mechanisms.
Main Results:
- MV infection alters membrane sphingolipid composition and metabolism.
- Sphingomyelin breakdown and ceramide release are regulated during MV infection.
- These alterations impact cellular interactions and immune cell functions.
Conclusions:
- Dysregulation of sphingomyelinase activity and ceramide release by MV contributes to immunosuppression.
- Targeting sphingolipid metabolism could be a strategy to mitigate measles-associated complications.
