AI Article Synopsis
- * The virus disrupts various immune functions, such as delayed-type hypersensitivity reactions, lymphocyte activity, and the production of important immune molecules like interleukin 12 and interferon.
- * This review discusses how specific MV proteins (like hemagglutinin and fusion protein) interact with cell receptors to contribute to these immune dysfunctions, highlighting recent findings in the field.
Article Abstract
Measles virus (MV) causes transient but profound immunosuppression resulting in increased susceptibility to secondary bacterial and viral infections. Due to the development of these opportunistic infections, measles remains the leading vaccine-preventable cause of child death worldwide. Different immune abnormalities have been associated with measles, including disappearance of delayed-type hypersensitivity reactions, impaired lymphocyte and antigen-presenting cell functions, down-regulation of pro-inflammatory interleukin 12 production and altered interferon alpha/beta signalling pathways. Several MV proteins have been suggested to hinder immune functions: hemagglutinin, fusion protein, nucleoprotein and the non-structural V and C proteins. This review will focus on the novel functions attributed to MV proteins in the immunosuppression associated with measles. Here, we highlight new advances in the field, emphasising the interaction between MV proteins and their cellular targets, in particular the cell membrane receptors, CD46, CD150, TLR2 and FcgammaRII in the induction of immunological abnormalities associated with measles.
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| http://dx.doi.org/10.1002/rmv.486 | DOI Listing |
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