Human Dendritic Cells as Targets of Dengue Virus Infection

Marovich, Mary; Grouard-Vogel, Géraldine; Louder, Mark K.; Eller, Michael A.; Sun, Wellington; Wu, Shuenn-Ju; Putvatana, Ravithat; Murphy, Gerald S.; Tassaneetrithep, Boonrat; Burgess, Timothy; Birx, Deborah L.; Hayes, Curtis G.; Schlesinger-Frankel, Sarah; Mascola, John R.

doi:10.1046/j.0022-202x.2001.00037.x

Cited by 153 publications

(142 citation statements)

References 21 publications

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“…Both CD209L and DC-SIGN mediate attachment of Sindbis glycoprotein via their CRDs and mediate productive infection by Sindbis virus, especially by virus produced in insect cells that has high levels of high mannose glycans on the envelope glycoproteins compared with virus produced in mammalian cells (30). DC-SIGN also mediates productive infection of human dendritic cells by dengue virus (31,32). DC-SIGN and CD209L glycoproteins bind hepatitis C virus glycoproteins E1 and E2 (33).…”

Section: Discussionmentioning

confidence: 99%

CD209L (L-SIGN) is a receptor for severe acute respiratory syndrome coronavirus

Jeffers

Tusell

Gillim-Ross

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

580

570

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Severe acute respiratory syndrome (SARS) is caused by a novel coronavirus called SARS-CoV (1-3). The virus causes atypical pneumonia with diffuse alveolar damage with an overall mortality of Ϸ10% that ranges from 0% in children and 50% in persons over 65 (2). Coronaviruses bind to their glycoprotein receptors by the Ϸ200-kDa spike glycoprotein, S, on the viral envelope. Identification of virus receptors can provide insight into mechanisms of virus entry, tissue tropism, pathogenesis, and host range.Several types of receptors were previously identified for coronavirus S glycoproteins. The receptors for the murine coronavirus mouse hepatitis virus are murine carcinoembryonic antigen cell adhesion molecule 1 (CEACAM1) and related murine glycoproteins in the carcinoembryonic antigen family in the Ig superfamily (4). The receptors for human coronavirus 229E (HCoV-229E), transmissible gastroenteritis virus of swine, and feline coronavirus in genetic group 1 are aminopeptidase N (APN) glycoproteins (5-8).Angiotensin-converting enzyme 2 (ACE2) was found to be an efficient receptor for the S glycoprotein of SARS-CoV (9, 10). Because the Vero line of rhesus monkey kidney cells is highly susceptible to infection with SARS-CoV, Li et al. (9) used a codon-optimized soluble SARS-CoV spike glycoprotein (amino acids 12-672) fused to the Fc domain of human IgG1 to immunoprecipitate a putative receptor glycoprotein from Vero cell membranes and identified the simian ACE2 protein by mass spectrometry. They showed that expression of recombinant human ACE2 greatly enhanced the susceptibility of human 293T cells to infection by SARS-CoV. Wang et al. (10) independently demonstrated that human ACE2 is a receptor for SARS-CoV by transducing HeLa cells with a retrovirus library of cDNAs from Vero E6 cells and by using flow cytometry to select transduced cells that bound to purified soluble SARS-CoV S glycoprotein (amino acids 14-502) with a 6-histidine tag. They found that the simian cDNA in these cells, which encoded triosephosphate isomerase, enhanced expression of human ACE2 by inserting into the HeLa cell genome immediately upstream of the ACE2 ORF. Murine NIH 3T3 cells expressing recombinant human ACE2, but not those expressing recombinant triosephosphate isomerase, were susceptible to infection by HIV pseudovirus expressing SARS-CoV S protein.In this report, we describe the discovery of an additional receptor for SARS-CoV, CD209L (also called L-SIGN, DC-SIGNR, and DC-SIGN2) (11). Our strategy for identifying a SARS-CoV receptor was to transduce a human lung cDNA library carried by a retroviral vector into Chinese hamster ovary (CHO) cells and use flow cytometry to select transduced CHO cells that bound soluble, codon-optimized, c-myc-tagged SARSCoV S 590 glycoprotein (amino acids 1-590) expressed in 293T cells. The SARS-CoV S 590 -binding cells were then challenged with infectious SARS-CoV, and infection was demonstrated by detection of subgenomic viral RNA synthesis and immunofluorescence with antiviral antibody. The finding that ...

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Section: Discussionmentioning

confidence: 99%

CD209L (L-SIGN) is a receptor for severe acute respiratory syndrome coronavirus

Jeffers

Tusell

Gillim-Ross

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

580

570

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“…Several studies demonstrated that dendritic cells (DCs) are more permissive to DV infection compared with monocytes and macrophages (3,4). DC-specific ICAM-3-grabbing nonintegrin (DC-SIGN), a cell surface C-type lectin expressed on DCs, plays a critical role in DV binding and infection (5,6).…”

Section: Engue Viruses (Dv)mentioning

confidence: 99%

CD40 Ligand Enhances Dengue Viral Infection of Dendritic Cells: A Possible Mechanism for T Cell-Mediated Immunopathology

Sun

Celluzzi

Marovich

et al. 2006

The Journal of Immunology

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We have previously shown that dengue virus (DV) productively infects immature human dendritic cells (DCs) through binding to cell surface DC-specific ICAM-3-grabbing nonintegrin molecules. Infected DCs are apoptotic, refractory to TNF-␣ stimulation, inhibited from undergoing maturation, and unable to stimulate T cells. In this study, we show that maturation of infected DCs could be restored by a strong stimulus, CD40L. Addition of CD40L significantly reduced apoptosis of DCs, promoted IL-12 production, and greatly elevated the IFN-␥ response of T cells, but yet did not restore T cell proliferation in MLR. Increased viral infection of DCs was also observed; however, increased infection did not appear to be mediated by DC-specific ICAM-3-grabbing nonintegrin, but rather was regulated by decreased production of IFN-␣ and decreased apoptotic death of infected DCs. Because CD40L is highly expressed on activated memory (but not naive) T cells, the observation that CD40L signaling results in enhanced DV infection of DC suggests a possible T cell-dependent mechanism for the immune-mediated enhancement of disease severity associated with some secondary dengue infections.

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“…Recently, our group demonstrated that the presence of a mutation affecting the DV1-NS3 hel protein (L435S or L480S) correlates with increased viral replicative capacity both in vitro and in vivo by increasing RNA synthesis and the viral load, as well as by enhancing the inflammatory profile and mouse mortality [34]. In the present study, we sought to investigate how the same DV1-NS3 hel -mutated strains (vBAC-NS3 435 or vBAC-NS3 480 ) could modulate response of the primary targets of DV infection, human mdDCs [47]. Dendritic cells play a key role as an innate immune cell, triggering adaptive immune responses [23,24,45].…”

Section: Discussionmentioning

confidence: 99%

Single point mutations in the helicase domain of the NS3 protein enhance dengue virus replicative capacity in human monocyte-derived dendritic cells and circumvent the type I interferon response

Silveira

Strottmann

Borba

et al. 2015

Clinical and Experimental Immunology

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SummaryDengue is the most prevalent arboviral disease worldwide. The outcome of the infection is determined by the interplay of viral and host factors. In the present study, we evaluated the cellular response of human monocytederived DCs (mdDCs) infected with recombinant dengue virus type 1 (DV1) strains carrying a single point mutation in the NS3 hel protein (L435S or L480S). Both mutated viruses infect and replicate more efficiently and produce more viral progeny in infected mdDCs compared with the parental, non-mutated virus (vBACDV1). Additionally, global gene expression analysis using cDNA microarrays revealed that the mutated DVs induce the up-regulation of the interferon (IFN) signalling and pattern recognition receptor (PRR) canonical pathways in mdDCs. Pronounced production of type I IFN were detected specifically in mdDCs infected with DV1-NS3 helmutated virus compared with mdDCs infected with the parental virus. In addition, we showed that the type I IFN produced by mdDCs is able to reduce DV1 infection rates, suggesting that cytokine function is effective but not sufficient to mediate viral clearance of DV1-NS3 hel -mutated strains. Our results demonstrate that single point mutations in subdomain 2 have important implications for adenosine triphosphatase (ATPase) activity of DV1-NS3 hel . Although a direct functional connection between the increased ATPase activity and viral replication still requires further studies, these mutations speed up viral RNA replication and are sufficient to enhance viral replicative capacity in human primary cell infection and circumvent type I IFN activity. This information may have particular relevance for attenuated vaccine protocols designed for DV.

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Human Dendritic Cells as Targets of Dengue Virus Infection

Cited by 153 publications

References 21 publications

CD209L (L-SIGN) is a receptor for severe acute respiratory syndrome coronavirus

CD209L (L-SIGN) is a receptor for severe acute respiratory syndrome coronavirus

CD40 Ligand Enhances Dengue Viral Infection of Dendritic Cells: A Possible Mechanism for T Cell-Mediated Immunopathology

Single point mutations in the helicase domain of the NS3 protein enhance dengue virus replicative capacity in human monocyte-derived dendritic cells and circumvent the type I interferon response

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