John Bisbing

Walter Reed Army Institute of Research

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Dupeh R. Palmer

Walter Reed Army Institute of Research

Wellington Sun

United States Food and Drug Administration

Vicky Gunther

Walter Reed Army Institute of Research

Dave Barvir

Walter Reed Army Institute of Research

Timothy Burgess

Uniformed Services University of the Health Sciences

Kristina K. Peachman

Walter Reed Army Institute of Research

Stefan Fernandez

Armed Forces Research Institute of Medical Science

Peifang Sun

Naval Medical Research Command

Mangala Rao

Walter Reed Army Institute of Research

Christina M. Celluzzi

American Association of Blood Banks

Cooperative Institutions

Walter Reed Army Institute of Research

Henry M. Jackson Foundation

Jackson Foundation

Naval Medical Research Command

United States Food and Drug Administration

Georgetown University

University of Maryland, Baltimore

Uniformed Services University of the Health Sciences

Johns Hopkins University

United States Department of the Navy

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Modulation of Dengue Virus Infection of Dendritic Cells byAedes aegyptiSaliva

Viral Immunology (2004)

Daniel B. Ader Christina M. Celluzzi John Bisbing Lara E. Gilmore Vicky Gunther

Dengue virus (DV) is a flavivirus carried by the Aedes aegypti mosquito that causes a spectrum of illnesses in the tropics, including dengue fever, dengue hemorrhagic fever, and dengue shock syndrome. Dendritic cells (DCs) are professional antigen presenting cells recently shown to be permissive for DV, and implicated as the primary targets of initial DV infection. DV is transmitted to human host by infected mosquitoes during a blood meal, but it is currently unknown whether transmission is modified by vector saliva that is also deposited in the host's skin during feeding. Previous studies evaluated only the outcome of DV infection of DCs, and did not address the influence of mosquito saliva. To more fully characterize natural transmission of DV, we evaluated the effects of Ae. aegypti saliva on DV infection of human myeloid DCs. We found that saliva inhibited DV infection in DCs. Moreover, pre-sensitization of DCs with saliva, prior to DV infection, enhanced inhibition. In addition, enhanced production of IL-12p70 and TNF-α were detected in DV-infected DC cultures exposed to mosquito saliva. The proportion of dead cells was also significantly reduced in these cultures. These data contribute to the overall understanding of the natural pathogenesis of DV infection and suggest that there is a protective role for mosquito saliva that limits viral uptake by DCs.

Flavivirus

Blood meal

10.1089/0882824041310496

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Restricted replication and lysosomal trafficking of yellow fever 17D vaccine virus in human dendritic cells

Journal of General Virology (2006)

Dupeh R. Palmer Stefan Fernandez John Bisbing Kristina K. Peachman Mangala Rao

The yellow fever virus attenuated 17D vaccine strain is a safe and effective vaccine and a valuable model system for evaluating immune responses against attenuated viral variants. This study compared the in vitro interactions of the commercially available yellow fever vaccine (YF-VAX), Dengue virus and the live-attenuated dengue vaccine PDK50 with dendritic cells (DCs), the main antigen-presenting cells at the initiation of immune responses. Similar to PDK50, infection with YF-VAX generated activated DCs; however, for YF-VAX, activation occurred with limited intracellular virus replication. The majority of internalized virus co-localized with endolysosomal markers within 90 min, suggesting that YF-VAX is processed rapidly in DCs. These results indicate that restricted virus replication and lysosomal compartmentalization may be important contributing factors to the success of the YF-VAX vaccine.

Yellow fever vaccine

Attenuated vaccine

10.1099/vir.0.82272-0

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Potential Role for Toll-Like Receptor 4 in Mediating Escherichia coli Maltose-Binding Protein Activation of Dendritic Cells

Infection and Immunity (2007)

Stefan Fernandez Dupeh R. Palmer Monika Simmons Peifang Sun John Bisbing

The Escherichia coli maltose-binding protein (MBP) is used to increase the stability and solubility of proteins in bacterial protein expression systems and is increasingly being used to facilitate the production and delivery of subunit vaccines against various pathogenic bacteria and viruses. The MBP tag is presumed inert, with minimum effects on the bioactivity of the tagged protein or its biodistribution. However, few studies have characterized the immunological attributes of MBP. Here, we analyze the phenotypic and functional outcomes of MBP-treated dendritic cells (DCs) and show that MBP induces DC activation and production of proinflammatory cytokines (interleukin-1beta [IL-1beta], IL-6, IL-8, tumor necrosis factor alpha, and IL-12p70) within 24 h and strongly increases Ikappabeta phosphorylation in treated cells. Interestingly, phosphorylation of Ikappabeta was largely abrogated by the addition of anti-human Toll-like receptor 4 (TLR4) antibodies, indicating that MBP activates signaling for DC maturation via TLR4. Consistent with this hypothesis, MBP activated the TLR4-expressing cell line 293-hTLR4A but not control cultures to secrete IL-8. The observed data were independent of lipopolysaccharide contamination and support a role for TLR4 in mediating the effects of MBP. These results provide insight into a mechanism by which MBP might enhance immune responses to vaccine fusion proteins.

Maltose-binding protein

Proinflammatory cytokine

10.1128/iai.00486-06

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Differential Effects of Dengue Virus on Infected and Bystander Dendritic Cells

Journal of Virology (2005)

Dupeh R. Palmer Peifang Sun Christina M. Celluzzi John Bisbing Somnang Pang

Dendritic cells (DCs) play a central role as major targets of dengue virus (DV) infections and initiators of antiviral immune responses. Previous observations showed that DCs are activated by infection, presumably acquiring the capacity to promote cell-mediated immunity. However, separate evaluations of the maturation profiles of infected and uninfected bystander cells show that infection impairs the ability of DCs to upregulate cell surface expression of costimulatory, maturation, and major histocompatibility complex molecules, resulting in reduced T-cell stimulatory capacity. Infected DCs failed to respond to tumor necrosis factor alpha as an additional maturation stimulus and were apoptotic. Interleukin 10 (IL-10) was detected in supernatants from cultures of DV-infected DCs and cocultures of DCs and T cells. Taken together, these results constitute an immune evasion strategy used by DV that directly impairs antigen-presenting cell function by maturation blockade and induction of apoptosis.

Bystander effect

10.1128/jvi.79.4.2432-2439.2005

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Citations (129)