scholarly journals Dengue virus infection and immune response in humanized RAG2−/−γc−/− (RAG-hu) mice

Virology ◽  
2007 ◽  
Vol 369 (1) ◽  
pp. 143-152 ◽  
Author(s):  
Jes G. Kuruvilla ◽  
Ryan M. Troyer ◽  
Shamala Devi ◽  
Ramesh Akkina
Keyword(s):  
Immune Response ◽  
Virus Infection ◽  
Dengue Virus ◽  
Dengue Virus Infection

scholarly journals Dendritic Cell Precursors Are Permissive to Dengue Virus and Human Immunodeficiency Virus Infection

2005 ◽  
Vol 79 (12) ◽  
pp. 7291-7299 ◽  
Author(s):  
Wing-Hong Kwan ◽  
Anna-Marija Helt ◽  
Concepción Marañón ◽  
Jean-Baptiste Barbaroux ◽  
Anne Hosmalin ◽  
...  
Keyword(s):  
Immune Response ◽  
Human Immunodeficiency Virus ◽  
Virus Infection ◽  
Dengue Virus ◽  
Blood Monocytes ◽  
Dengue Virus Infection ◽  
Differentiation Potential ◽  
Antiviral Immune Response ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT CD14+ interstitial cells reside beneath the epidermis of skin and mucosal tissue and may therefore play an important role in viral infections and the shaping of an antiviral immune response. However, in contrast to dendritic cells (DC) or blood monocytes, these antigen-presenting cells (APC) have not been well studied. We have previously described long-lived CD14+ cells generated from CD34+ hematopoietic progenitors, which may represent model cells for interstitial CD14+ APC. Here, we show that these cells carry DC-SIGN and differentiate into immature DC in the presence of granulocyte-macrophage colony-stimulating factor. We have compared the CD14+ cells and the DC derived from these cells with respect to dengue virus and human immunodeficiency virus type 1 (HIV-1) infection. Both cell types are permissive to dengue virus infection, but the CD14+ cells secrete the anti-inflammatory cytokine interleukin 10 and no tumor necrosis factor alpha. Regarding HIV, the CD14+ cells are permissive to HIV-1, release higher p24 levels than the derived DC, and more efficiently activate HIV Pol-specific CD8+ memory T cells. The CD14+ DC precursors infected with either virus retain their DC differentiation potential. The results suggest that interstitial CD14+ APC may contribute to HIV-1 and dengue virus infection and the shaping of an antiviral immune response.

scholarly journals Current Understanding of the Pathogenesis of Dengue Virus Infection

2020 ◽  
Author(s):  
Puneet Bhatt ◽  
Sasidharan Pillai Sabeena ◽  
Muralidhar Varma ◽  
Govindakarnavar Arunkumar
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Virus Infection ◽  
Dengue Virus ◽  
Genetic Factors ◽  
Host Immune Response ◽  
Severe Dengue ◽  
Ns1 Protein ◽  
Dengue Virus Infection ◽  
Antibody Dependent Enhancement

AbstractThe pathogenesis of dengue virus infection is attributed to complex interplay between virus, host genes and host immune response. Host factors such as antibody-dependent enhancement (ADE), memory cross-reactive T cells, anti-DENV NS1 antibodies, autoimmunity as well as genetic factors are major determinants of disease susceptibility. NS1 protein and anti-DENV NS1 antibodies were believed to be responsible for pathogenesis of severe dengue. The cytokine response of cross-reactive CD4+ T cells might be altered by the sequential infection with different DENV serotypes, leading to further elevation of pro-inflammatory cytokines contributing a detrimental immune response. Fcγ receptor-mediated antibody-dependent enhancement (ADE) results in release of cytokines from immune cells leading to vascular endothelial cell dysfunction and increased vascular permeability. Genomic variation of dengue virus and subgenomic flavivirus RNA (sfRNA) suppressing host immune response are viral determinants of disease severity. Dengue infection can lead to the generation of autoantibodies against DENV NS1antigen, DENV prM, and E proteins, which can cross-react with several self-antigens such as plasminogen, integrin, and platelet cells. Apart from viral factors, several host genetic factors and gene polymorphisms also have a role to play in pathogenesis of DENV infection. This review article highlights the various factors responsible for the pathogenesis of dengue and also highlights the recent advances in the field related to biomarkers which can be used in future for predicting severe disease outcome.

scholarly journals Altered immune response of immature dendritic cells following dengue virus infection in the presence of specific antibodies

2016 ◽  
Vol 97 (7) ◽  
pp. 1584-1591 ◽  
Author(s):  
Silvia Torres ◽  
Jacky Flipse ◽  
Vinit C. Upasani ◽  
Heidi van der Ende-Metselaar ◽  
Silvio Urcuqui-Inchima ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Virus Infection ◽  
Dengue Virus ◽  
Dengue Virus Infection ◽  
Specific Antibodies ◽  
Immature Dendritic Cells ◽  
Altered Immune Response

scholarly journals Human Dendritic Cells Are Activated by Dengue Virus Infection: Enhancement by Gamma Interferon and Implications for Disease Pathogenesis

2001 ◽  
Vol 75 (8) ◽  
pp. 3501-3508 ◽  
Author(s):  
Daniel H. Libraty ◽  
Sathit Pichyangkul ◽  
Chuanpis Ajariyakhajorn ◽  
Timothy P. Endy ◽  
Francis A. Ennis
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Virus Infection ◽  
Dengue Virus ◽  
Adaptive Immune Response ◽  
Interleukin 12 ◽  
Cell Mediated Immunity ◽  
Dengue Virus Infection ◽  
Adaptive Immune ◽  
Ifn Γ

ABSTRACT The ability of dendritic cells (DCs) to shape the adaptive immune response to viral infection is mediated largely by their maturation and activation state as determined by the surface expression of HLA molecules, costimulatory molecules, and cytokine production. Dengue is an emerging arboviral disease where the severity of illness is influenced by the adaptive immune response to the virus. In this report, we have demonstrated that dengue virus infects and replicates in immature human myeloid DCs. Exposure to live dengue virus led to maturation and activation of both the infected and surrounding, uninfected DCs and stimulated production of tumor necrosis factor alpha (TNF-α) and alpha interferon (IFN-α). Activation of the dengue virus-infected DCs was blunted compared to the surrounding, uninfected DCs, and dengue virus infection induced low-level release of interleukin-12 p70 (IL-12 p70), a key cytokine in the development of cell-mediated immunity (CMI). Upon the addition of IFN-γ, there was enhanced activation of dengue virus-infected DCs and enhanced dengue virus-induced IL-12 p70 release. The data suggest a model whereby DCs are the early, primary target of dengue virus in natural infection and the vigor of CMI is modulated by the relative presence or absence of IFN-γ in the microenvironment surrounding the virus-infected DCs. These findings are relevant to understanding the pathogenesis of dengue hemorrhagic fever and the design of new vaccination and therapeutic strategies.

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