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Updated: Feb 12, 2026

Early Viral Entry Assays for the Identification and Evaluation of Antiviral Compounds
Published on: October 29, 2015
C-Type Lectin Receptors in Antiviral Immunity and Viral Escape
Marta Bermejo-Jambrina1,2, Julia Eder1, Leanne C Helgers1
1Department of Experimental Immunology, Amsterdam Infection and Immunity Institute, Academic Medical Center, University of Amsterdam, Amsterdam, Netherlands.
Abstract:
C-type lectin receptors (CLRs) are important pattern recognition receptors involved in recognition and induction of adaptive immunity to pathogens. Certain CLRs play an important role in viral infections as they efficiently interact with viruses. However, it has become clear that deadly viruses subvert the function of CLRs to escape antiviral immunity and promote infection. In particular, viruses target CLRs to suppress or modulate type I interferons that play a central role in the innate and adaptive defense against viruses. In this review, we discuss the function of CLRs in binding to enveloped viruses like HIV-1 and Dengue virus, and how uptake and signaling cascades have decisive effects on the outcome of infection.
Insights
Deadly viruses hijack C-type lectin receptors (CLRs) to evade immune responses. This review explores how viruses like HIV-1 and Dengue virus manipulate CLR function, impacting antiviral defenses and infection outcomes.
Area of Science:
- Immunology
- Virology
- Molecular Biology
Background:
- C-type lectin receptors (CLRs) are crucial pattern recognition receptors mediating innate immunity against pathogens.
- Viruses, including enveloped viruses like HIV-1 and Dengue virus, interact with CLRs.
- Viruses have evolved mechanisms to subvert CLR functions, thereby evading host antiviral responses.
Purpose of the Study:
- To review the multifaceted roles of CLRs in viral infections.
- To elucidate how viruses exploit CLRs to suppress or modulate critical antiviral pathways, particularly type I interferons.
- To discuss the impact of CLR-mediated viral uptake and signaling on infection outcomes.
Main Methods:
- Literature review focusing on CLR-pathogen interactions in viral infections.
- Analysis of studies investigating CLR binding to enveloped viruses.
- Examination of research on viral subversion of CLR-dependent signaling cascades.
Main Results:
- CLRs are key players in recognizing and initiating immune responses to viruses.
- Many viruses, such as HIV-1 and Dengue virus, are recognized by specific CLRs.
- Viruses actively manipulate CLR function to impair type I interferon responses and promote viral spread.
Conclusions:
- CLR interactions with viruses are critical determinants of infection outcome.
- Understanding viral subversion of CLRs offers potential targets for antiviral therapies.
- Targeting CLR-mediated pathways could enhance innate and adaptive immunity against viral pathogens.
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