The monocyte-macrophage-mast cell axis in dengue pathogenesis

Wan, Shu; Wu-Hsieh, Betty A.; Lin, Yee Shin; Chen, Wen Yu; Huang, Yan; Anderson, Robert

doi:10.1186/s12929-018-0482-9

Cited by 45 publications

(39 citation statements)

References 109 publications

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“…Also, it has been possible to produce vascular permeability in DENV-infected infant mice born to dengue-immune mothers 82 . But other hypotheses of severe dengue pathogenesis that attribute disease (1) to a weakened ability of secondary T cells to contain DENV infection because of the original antigenic sin phenomenon, (2) to the hyper-production of endothelium-damaging secondary infection T-cell cytokines and chemokines, (3) to the DENV non-structural protein 1 (NS1) heterophile antibodies raised during first DENV infections that damage platelets, endothelial cells, or blood clotting proteins during second infections, or (4) to the ability of dengue IgG immune complexes to stimulate mast cells to release vasoactive amines fail to satisfy the requirements of Occam’s razor 83– 86 . None of these hypotheses explains the phenomenon of infant DVPS where B- and T-cell responses are primary and anti-DENV or anti-NS1 IgG antibody concentrations at the onset of illness are absent or very low.…”

Section: Pathogenesismentioning

confidence: 99%

Recent advances in understanding dengue

Halstead

2019

F1000Res

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This is a selective review of recent publications on dengue clinical features, epidemiology, pathogenesis, and vaccine development placed in a context of observations made over the past half century. Four dengue viruses (DENVs) are transmitted by urban cycle mosquitoes causing diseases whose nature and severity are influenced by interacting factors such as virus, age, immune status of the host, and human genetic variability. A phenomenon that controls the kinetics of DENV infection, antibody-dependent enhancement, best explains the correlation of the vascular permeability syndrome with second heterotypic DENV infections and infection in the presence of passively acquired antibodies. Based on growing evidence in vivo and in vitro, the tissue-damaging DENV non-structural protein 1 (NS1) is responsible for most of the pathophysiological features of severe dengue. This review considers the contribution of hemophagocytic histiocytosis syndrome to cases of severe dengue, the role of movement of humans in dengue epidemiology, and modeling and planning control programs and describes a country-wide survey for dengue infections in Bangladesh and efforts to learn what controls the clinical outcome of dengue infections. Progress and problems with three tetravalent live-attenuated vaccines are reviewed. Several research mysteries remain: why is the risk of severe disease during second heterotypic DENV infection so low, why is the onset of vascular permeability correlated with defervescence, and what are the crucial components of protective immunity?

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Section: Pathogenesismentioning

confidence: 99%

Recent advances in understanding dengue

Halstead

2019

F1000Res

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“…Macrophages play a critical role in the induction and regulation of both innate and adaptive immune responses and sometimes act as a double-edged sword during certain viral infections, including flavivirus infections, as macrophages may not only help fight against viral infection but also contribute to virus production and dissemination during viral infections (14)(15)(16)(17)(18). The interactions between host macrophages and a number of viruses have been extensively studied in mammal models.…”

mentioning

confidence: 99%

Avian Flavivirus Infection of Monocytes/Macrophages by Extensive Subversion of Host Antiviral Innate Immune Responses

Liang

Wang

et al. 2019

J Virol

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Avian Tembusu virus (TMUV) is a newly emerging avian pathogenic flavivirus in China and Southeast Asia with features of rapid spread, an expanding host range, and cross-species transmission. The mechanisms of its infection and pathogenesis remain largely unclear. Here, we investigated the tropism of this arbovirus in peripheral blood mononuclear cells of specific-pathogen-free (SPF) ducks and SPF chickens and identified monocytes/macrophages as the key targets of TMUV infection. In vivo studies in SPF ducks and SPF chickens with monocyte/macrophage clearance demonstrated that the infection of monocytes/macrophages was crucial for viral replication, transmission, and pathogenesis. Further genome-wide transcriptome analyses of TMUV-infected chicken macrophages revealed that host antiviral innate immune barriers were the major targets of TMUV in macrophages. Despite the activation of major pattern recognition receptor signaling, the inductions of alpha interferon (IFN-α) and IFN-β were blocked by TMUV infection on transcription and translation levels, respectively. Meanwhile, TMUV inhibited host redox responses by repressing the transcription of genes encoding NADPH oxidase subunits and promoting Nrf2-mediated antioxidant responses. The recovery of either of the above-mentioned innate immune barriers was sufficient to suppress TMUV infection. Collectively, we identify an essential step of TMUV infection and reveal extensive subversion of host antiviral innate immune responses. IMPORTANCE Mosquito-borne flaviviruses include a group of pathogenic viruses that cause serious diseases in humans and animals, including dengue, West Nile, and Japanese encephalitis viruses. These flaviviruses are zoonotic and use animals, including birds, as amplifying and reservoir hosts. Avian Tembusu virus (TMUV) is an emerging mosquito-borne flavivirus that is pathogenic for many avian species and can infect cells derived from mammals and humans in vitro. Although not currently pathogenic for primates, the infection of duck industry workers and the potential risk of TMUV infection in immunocompromised individuals have been highlighted. Thus, the prevention of TMUV in flocks is important for both avian and mammalian health. Our study reveals the escape of TMUV from the first line of the host defense system in the arthropod-borne transmission route of arboviruses, possibly helping to extend our understanding of flavivirus infection in birds and refine the design of anti-TMUV therapeutics.

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“…MCs contribute to a response to infection that involves multiple cell types. In addition to MC endothelial cell interactions, the interface between dengue virus, monocytes and macrophages and MCs may be of particular importance [47]. Notably, MC infection with hantavirus has also been associated with a similar mediator response that may contribute to vascular dysfunction [48].…”

Section: Mast Cells and Mosquito-borne Virusesmentioning

confidence: 99%

Mast Cell Responses to Viruses and Pathogen Products

Marshall

Portales‐Cervantes

Leong

2019

IJMS

124

133

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Mast cells are well accepted as important sentinel cells for host defence against selected pathogens. Their location at mucosal surfaces and ability to mobilize multiple aspects of early immune responses makes them critical contributors to effective immunity in several experimental settings. However, the interactions of mast cells with viruses and pathogen products are complex and can have both detrimental and positive impacts. There is substantial evidence for mast cell mobilization and activation of effector cells and mobilization of dendritic cells following viral challenge. These cells are a major and under-appreciated local source of type I and III interferons following viral challenge. However, mast cells have also been implicated in inappropriate inflammatory responses, long term fibrosis, and vascular leakage associated with viral infections. Progress in combating infection and boosting effective immunity requires a better understanding of mast cell responses to viral infection and the pathogen products and receptors we can employ to modify such responses. In this review, we outline some of the key known responses of mast cells to viral infection and their major responses to pathogen products. We have placed an emphasis on data obtained from human mast cells and aim to provide a framework for considering the complex interactions between mast cells and pathogens with a view to exploiting this knowledge therapeutically. Long-lived resident mast cells and their responses to viruses and pathogen products provide excellent opportunities to modify local immune responses that remain to be fully exploited in cancer immunotherapy, vaccination, and treatment of infectious diseases.

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The monocyte-macrophage-mast cell axis in dengue pathogenesis

Cited by 45 publications

References 109 publications

Recent advances in understanding dengue

Recent advances in understanding dengue

Avian Flavivirus Infection of Monocytes/Macrophages by Extensive Subversion of Host Antiviral Innate Immune Responses

Mast Cell Responses to Viruses and Pathogen Products

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