DC-SIGN enhances infection of cells with glycosylated West Nile virus in vitro and virus replication in human dendritic cells induces production of IFN-α and TNF-α

Martina, Benedict; Koraka, Penelope; Doel, Petra van den; Rimmelzwaan, Guus F.; Haagmans, Bart L.; Osterhaus, Albert D. M. E.

doi:10.1016/j.virusres.2008.02.008

Cited by 66 publications

(50 citation statements)

References 33 publications

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“…E protein glycosylation has been linked to increased virulence in mammalian and avian models of infection (Beasley et al, 2005;Brault et al, 2011;Kariwa et al, 2013;Murata et al, 2010;Shirato et al, 2004b;Totani et al, 2011) and efficient transmission by mosquitoes (Moudy et al, 2009). Glycosylation at the E protein is proposed to potentiate these virulence phenotypes by facilitating receptor-mediated virus entry (Davis et al, 2006a, b;Martina et al, 2008;Mondotte et al, 2007;Pokidysheva et al, 2006;Tassaneetrithep et al, 2003), a greater efficiency of particle assembly and egress (Goto et al, 2005;Hanna et al, 2005;Lee et al, 2010;Li et al, 2006;Scherret et al, 2001), increased pH stability (Beasley et al, 2005;Guirakhoo et al, 1993;Lee et al, 1997) and possibly the concealment of immunogenic epitopes (Zhang et al, 2011).…”

Section: Glycan Modificationmentioning

confidence: 99%

“…Two of the best-characterized receptors for flaviviruses rely almost solely on glycosylation of the E protein for interaction (and prM in immature/partially mature virions): the type II tetrameric transmembrane proteins containing Ca 2+ -dependent carbohydrate recognition domains DC-SIGN and DC-SIGNR (Davis et al, 2006a, b;FernandezGarcia et al, 2009;Martina et al, 2008;Mondotte et al, 2007;Pokidysheva et al, 2006;Tassaneetrithep et al, 2003). Dendritic cells and macrophages express DC-SIGN in humans, with homologous Ca 2+ -dependent (C-type) lectin receptors (CLRs) in mice displaying distinct patterns of expression (Koppel et al, 2005;Kwan et al, 2008;Navarro-Sanchez et al, 2003;Tassaneetrithep et al, 2003).…”

Section: Glycan Modificationmentioning

confidence: 99%

“…Dendritic cells and macrophages express DC-SIGN in humans, with homologous Ca 2+ -dependent (C-type) lectin receptors (CLRs) in mice displaying distinct patterns of expression (Koppel et al, 2005;Kwan et al, 2008;Navarro-Sanchez et al, 2003;Tassaneetrithep et al, 2003). This lectin receptor recognizes high-mannose glycans and fructose-containing Lewis x antigens (Koppel et al, 2005) and has been demonstrated as a primary cellular attachment moiety for DENV and WNV (Davis et al, 2006a, b;Kwan et al, 2008;Lozach et al, 2005;Martina et al, 2008;Navarro-Sanchez et al, 2003;Tassaneetrithep et al, 2003;Wang et al, 2011). Polymorphisms within the promoter encoding DC-SIGN have also been associated with severe TBEV infection in humans (Barkhash et al, 2012).…”

Section: Glycan Modificationmentioning

confidence: 99%

“…This is supported by experiments that demonstrated increased WNV binding to DC-SIGN when the E protein was mutated to introduce glycosylation at residue 67 (Davis et al, 2006a). However, this may not represent the sole means for glycosylated flaviviruses to interact with DC-SIGN as it does not account for the observed impact of polymorphisms on TBEV infection (Barkhash et al, 2012) or the ability of WT glycosylated WNV to use it as a receptor (Davis et al, 2006b;Martina et al, 2008), as both viruses only contain the N154 glycan. It may be that high-mannose glycosylation of arthropodderived flavivirus virions facilitates better DC-SIGN interaction with the N153/4 residue (Davis et al, 2006b;Navarro-Sanchez et al, 2003).…”

Section: Glycan Modificationmentioning

confidence: 99%

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Post-translational regulation and modifications of flavivirus structural proteins

Roby

Setoh

Hall

et al. 2015

Journal of General Virology

102

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Flaviviruses are a group of single-stranded, positive-sense RNA viruses that generally circulate between arthropod vectors and susceptible vertebrate hosts, producing significant human and veterinary disease burdens. Intensive research efforts have broadened our scientific understanding of the replication cycles of these viruses and have revealed several elegant and tightly co-ordinated post-translational modifications that regulate the activity of viral proteins. The three structural proteins in particular -capsid (C), pre-membrane (prM) and envelope (E) -are subjected to strict regulatory modifications as they progress from translation through virus particle assembly and egress. The timing of proteolytic cleavage events at the C-prM junction directly influences the degree of genomic RNA packaging into nascent virions. Proteolytic maturation of prM by host furin during Golgi transit facilitates rearrangement of the E proteins at the virion surface, exposing the fusion loop and thus increasing particle infectivity. Specific interactions between the prM and E proteins are also important for particle assembly, as prM acts as a chaperone, facilitating correct conformational folding of E. It is only once prM/E heterodimers form that these proteins can be secreted efficiently. The addition of branched glycans to the prM and E proteins during virion transit also plays a key role in modulating the rate of secretion, pH sensitivity and infectivity of flavivirus particles. The insights gained from research into post-translational regulation of structural proteins are beginning to be applied in the rational design of improved flavivirus vaccine candidates and make attractive targets for the development of novel therapeutics. FlavivirusesThe genus Flavivirus in the family Flaviviridae comprises small, enveloped viruses with non-segmented genomes consisting of single-stranded, positive-sense RNA. These RNA genomes are flanked by 59 and 39 untranslated regions (UTRs) and encode a single polyprotein that is cleaved coand post-translationally to generate between 10 and 11 viral proteins. The 59 UTR contains a type 1 m 7 GpppNm cap structure and the 39 UTR lacks a polyadenylated tail. Structural elements within the UTRs regulate genome replication, translation and host immune responses. Viral proteins are divided between structural proteins, which form the virion, and non-structural proteins, which are involved in genomic replication and modulating host immunity (Fig. 1a) (Lindenbach et al., 2007;Roby et al., 2012).Flaviviruses are maintained predominantly in natural transmission cycles between vertebrate reservoir species (normally mammalian or avian) and haematophagous arthropod vectors (mosquitoes or ticks). Notable exceptions are the viruses that are maintained solely in mosquito hosts (insectspecific flaviviruses) and viruses with no known invertebrate vector (Cook et al., 2012;Mackenzie et al., 2004). As of 2013, the International Committee on Taxonomy of Viruses has classified 53 different viral species as belonging to ...

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Section: Glycan Modificationmentioning

confidence: 99%

Section: Glycan Modificationmentioning

confidence: 99%

Section: Glycan Modificationmentioning

confidence: 99%

Section: Glycan Modificationmentioning

confidence: 99%

See 2 more Smart Citations

Post-translational regulation and modifications of flavivirus structural proteins

Roby

Setoh

Hall

et al. 2015

Journal of General Virology

102

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“…The glycosylation status of the E protein of WNV correlates with murine neuroinvasive phenotypes, with reduced viral entry into the CNS being evident for nonglycosylated and/or mutagenized viruses. The reduced neuroinvasive properties have been hypothesized to result from altered tropism, increased sensitivity to low-pH conditions in endocytic vesicles and a reduced affinity for receptors such as DC-SIGN for infection of monocytes/macrophages [13,31,94,115,155].…”

Section: Viral Determinants Of Flavivirus Encephalitismentioning

confidence: 99%

The contribution of rodent models to the pathological assessment of flaviviral infections of the central nervous system

2012

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Members of the genus Flavivirus are responsible for a spectrum of important neurological syndromes in humans and animals. Rodent models have been used extensively to model flavivirus neurological disease, to discover host-pathogen interactions that influence disease outcome, and as surrogates to determine the efficacy and safety of vaccines and therapeutics. In this review, we discuss the current understanding of flavivirus neuroinvasive disease and outline the host, viral and experimental factors that influence the outcome and reliability of virus infection of smallanimal models.

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Pathogenesis of West Nile Virus in Humans

Vandergaast

Hussmann

Fredericksen

2015

Human Emerging and Re‐emerging Infections

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DC-SIGN enhances infection of cells with glycosylated West Nile virus in vitro and virus replication in human dendritic cells induces production of IFN-α and TNF-α

Cited by 66 publications

References 33 publications

Post-translational regulation and modifications of flavivirus structural proteins

Post-translational regulation and modifications of flavivirus structural proteins

The contribution of rodent models to the pathological assessment of flaviviral infections of the central nervous system

Pathogenesis of West Nile Virus in Humans

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