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The morbillivirus receptor SLAM (CD150)
Hironobu Tatsuo1, Yusuke Yanagi
1Department of Virology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Abstract:
Morbilliviruses are highly contagious pathogens that cause some of the most devastating viral diseases of humans and animals, including measles virus (MV), canine distemper virus (CDV), and rinderpest virus (RPV). They replicate mainly in lymphoid organs throughout the body and cause severe immunosuppression accompanied with lymphopenia. We have recently shown that human, canine, and bovine signaling lymphocyte activation molecules (SLAMs; also known as CD150) act as cellular receptors for MV, CDV, and RPV, respectively. In these three morbilliviruses, all strains examined were shown to use SLAMs of their respective host species, and laboratory strains passaged on SLAM-negative cells were found to use, besides SLAM, alternative receptors, such as human CD46 for the Edmonston strain of MV. The use of SLAM as a receptor may be a property common to most, if not all, of the members of morbilliviruses. Human SLAM is a membrane glycoprotein selectively expressed on the cells of the immune system (immature thymocytes, activated lymphocytes, activated monocytes, and mature dendritic cells) and seems to mediate lymphocyte activation and to control interferon-gamma production. The destruction and/or impairment of infected SLAM-positive cells may be a mechanism for the immunosuppression induced by morbilliviruses, but other mechanisms may be also involved.
Insights
Signaling lymphocyte activation molecules (SLAMs) are key receptors for morbilliviruses like measles. This viral entry mechanism may explain how these pathogens cause severe immunosuppression in hosts.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Morbilliviruses are highly contagious pathogens responsible for severe human and animal diseases, such as measles, canine distemper, and rinderpest.
- These viruses replicate in lymphoid organs, leading to profound immunosuppression and lymphopenia.
- The cellular receptors utilized by morbilliviruses have been a critical area of investigation for understanding viral pathogenesis.
Purpose of the Study:
- To investigate the role of Signaling Lymphocyte Activation Molecules (SLAMs), also known as CD150, as cellular receptors for morbilliviruses.
- To explore the implications of SLAM usage for morbillivirus entry and the resultant immunosuppression.
- To determine if SLAM is a common receptor for a broad range of morbilliviruses.
Main Methods:
- Experimental determination of cellular receptor usage for measles virus (MV), canine distemper virus (CDV), and rinderpest virus (RPV).
- Analysis of viral strain adaptation and receptor switching in laboratory passaging experiments.
- Characterization of human SLAM expression patterns on immune cells.
Main Results:
- Human, canine, and bovine SLAMs were identified as cellular receptors for MV, CDV, and RPV, respectively.
- All examined morbillivirus strains utilized host SLAMs, with some laboratory strains adapting to alternative receptors like CD46.
- Human SLAM is expressed on immune cells and plays a role in lymphocyte activation and interferon-gamma regulation.
Conclusions:
- SLAM serves as a primary cellular receptor for multiple morbilliviruses, suggesting a conserved viral entry mechanism.
- The impairment or destruction of SLAM-positive immune cells is a likely contributor to morbillivirus-induced immunosuppression.
- Understanding SLAM-mediated viral entry provides insights into morbillivirus pathogenesis and potential therapeutic targets.
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