Abstract
Dengue is a mosquito-borne viral disease causing significant health and economic burdens globally. The dengue virus (DENV) comprises four serotypes (DENV1-4). Usually, the primary infection is asymptomatic or causes mild dengue fever (DF), while secondary infections with a different serotype increase the risk of severe dengue disease (dengue hemorrhagic fever, DHF). Complement system activation induces inflammation and tissue injury, contributing to disease pathogenesis. However, in asymptomatic or primary infections, protective immunity largely results from the complement system’s lectin pathway (LP), which is activated through foreign glycan recognition. Differences in N-glycans displayed on the DENV envelope membrane influence the lectin pattern recognition receptor (PRR) binding efficiency. The important PRR, mannan binding lectin (MBL), mediates DENV neutralization through (1) a complement activation-independent mechanism via direct MBL glycan recognition, thereby inhibiting DENV attachment to host target cells, or (2) a complement activation-dependent mechanism following the attachment of complement opsonins C3b and C4b to virion surfaces. The serum concentrations of lectin PRRs and their polymorphisms influence these LP activities. Conversely, to escape the LP attack and enhance the infectivity, DENV utilizes the secreted form of nonstructural protein 1 (sNS1) to counteract the MBL effects, thereby increasing viral survival and dissemination.
Highlights
Dengue is an insect-borne viral infection transmitted to humans from the bites of infected Aedes mosquitoes
High levels of the complement anaphylatoxins (C3a and C5a) and the terminal complement complex were present in the plasma of patients with severe dengue during a second infection with a different serotype, suggesting an association between complement activation and dengue severity [34,35,36,37]. These findings suggest that complement overactivation plays a role in dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS) pathogenesis
Asn-67 in mammalian cell-derived WNV improved mannan binding lectin (MBL) binding and the neutralization of the virus by MBL [47,51]. These findings suggest that MBL binding to flaviviruses is likely modulated by the number and processing of carbohydrates on the N-linked glycans of the Unlike WNV, the MBL-mediated neutralization of mammalian cell-derived dengue virus (DENV)
Summary
Dengue is an insect-borne viral infection transmitted to humans from the bites of infected Aedes mosquitoes. High levels of the complement anaphylatoxins (C3a and C5a) and the terminal complement complex (sC5b-9) were present in the plasma of patients with severe dengue during a second infection with a different serotype, suggesting an association between complement activation and dengue severity [34,35,36,37] These findings suggest that complement overactivation plays a role in DHF/DSS pathogenesis. NS1, a major secreted viral protein produced from infected cells, can bind to the surface of uninfected cells via an interaction with glycosaminoglycans [45], which can form immune complexes with specific antibodies purified from patients’ plasma This can trigger complement activation, as evident by C3dg and C5b-9 deposition (our unpublished data). We will focus on the role of the lectin pathway of complement activation in DENV
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