Receptor interactions, tropism, and mechanisms involved in morbillivirus-induced immunomodulation

Area of Science:

• Virology
• Immunology
• Cell Biology

Background:

• Morbilliviruses, including measles virus (MV), rinderpest virus (RPV), and canine distemper virus (CDV), are known to induce significant immunomodulation and immunosuppression in their hosts.
• The tropism of these viruses for immune cells is largely determined by their primary uptake receptor, signaling lymphocytic activation molecule (SLAM, also known as CD150).

Purpose of the Study:

• This review aims to discuss the complex receptor interactions, viral tropism, and underlying mechanisms responsible for the severe, yet transient, immunosuppression induced by MV and related morbilliviruses.
• To elucidate how various cell surface receptors contribute to viral pathogenesis and immune system modulation.

Main Methods:

• This review synthesizes existing literature on morbillivirus-host interactions.
• Analysis of studies detailing viral entry mechanisms and immune cell responses.
• Discussion of the roles of known and uncharacterized cell surface receptors.

Main Results:

• SLAM (CD150) is crucial for morbillivirus entry into immune cells, dictating viral tropism and systemic spread to organs like lymphoid tissues, skin, respiratory tract, and brain.
• Beyond SLAM, other receptors including substance P receptor, DC-SIGN, Toll-like receptors (TLR), Fc-gamma receptor II (FcgammaRII), and CD46, play diverse roles in modulating immune cell functions.
• These interactions lead to varied immunomodulatory effects, impacting immune cell viability, differentiation, trafficking, and effector functions.

Conclusions:

• Morbillivirus-induced immunosuppression is a multifaceted process involving interactions with multiple cell surface receptors.
• Understanding these receptor-virus interactions is critical for comprehending viral pathogenesis and developing therapeutic strategies against morbillivirus infections.