For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
8
views
37
references
 Top references
cited by
6
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      426
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Dengue Virus Infects Primary Human Hair Follicle Dermal Papilla Cells

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          During the epidemic of the dengue virus (DENV) infection in Taiwan in 2014 and 2015, we observed an abnormally high frequency of increased scalp hair shedding in infected individuals that could not be explained by telogen effluvium. In this study, the mechanism of hair loss caused by DENV was explored. Human hair follicle dermal papilla cells (HFDPCs) are essential for hair follicle morphogenesis and cycling. Thus, we established an in vitro DENV infection model in HFDPCs. On immunofluorescence analysis, HFDPCs that were susceptible to DENV infection responded to type I interferon (IFN) treatment, and the cells showed antibody-dependent enhancement (ADE) effect. The expression of the pro-inflammatory cytokines, interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-α), revealed an inflammatory response in DENV-infected HFDPCs. In particular, DENV infection impaired cell viability, and it activated caspase-associated cell death signaling in HFDPCs. In conclusion, our data indicate that direct infection with DENV causes inflammation and cell death in HFDPCs, which is involved in the mechanisms of hair loss after DENV infection. The knowledge of DENV infection in an immune-privileged tissue, such as hair follicles, may suggest their use for further studies on post-dengue fatigue syndrome (PDFS).

          Related collections

          Most cited references37

          • Record: found
          • Abstract: found
          • Article: not found

          Dengue virus pathogenesis: an integrated view.

          Byron Martina, Penelope Koraka, Albert Osterhaus (2009)
          Much remains to be learned about the pathogenesis of the different manifestations of dengue virus (DENV) infections in humans. They may range from subclinical infection to dengue fever, dengue hemorrhagic fever (DHF), and eventually dengue shock syndrome (DSS). As both cell tropism and tissue tropism of DENV are considered major determinants in the pathogenesis of dengue, there is a critical need for adequate tropism assays, animal models, and human autopsy data. More than 50 years of research on dengue has resulted in a host of literature, which strongly suggests that the pathogenesis of DHF and DSS involves viral virulence factors and detrimental host responses, collectively resulting in abnormal hemostasis and increased vascular permeability. Differential targeting of specific vascular beds is likely to trigger the localized vascular hyperpermeability underlying DSS. A personalized approach to the study of pathogenesis will elucidate the basis of individual risk for development of DHF and DSS as well as identify the genetic and environmental bases for differences in risk for development of severe disease.
          Article 0 comments Cited 318 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Localization of dengue virus in naturally infected human tissues, by immunohistochemistry and in situ hybridization.

            Kala Jessie, Mun Yik Fong, Shamala Devi … (2004)
            Dengue viral antigens have been demonstrated in several types of naturally infected human tissues, but little is known of whether these same tissues have detectable viral RNA. We studied tissue specimens from patients with serologically or virologically confirmed dengue infections by immunohistochemistry (IHC) and in situ hybridization (ISH), to localize viral antigen and RNA, respectively. IHC was performed on specimens obtained from 5 autopsies and 24 biopsies and on 20 blood-clot samples. For ISH, antisense riboprobes to the dengue E gene were applied to tissue specimens in which IHC was positive. Viral antigens were demonstrated in Kupffer and sinusoidal endothelial cells of the liver; macrophages, multinucleated cells, and reactive lymphoid cells in the spleen; macrophages and vascular endothelium in the lung; kidney tubules; and monocytes and lymphocytes in blood-clot samples. Positive-strand viral RNA was detected in the same IHC-positive cells found in the spleen and blood-clot samples. The strong, positive ISH signal in these cells indicated a high copy number of viral RNA, suggesting replication.
            Article 0 comments Cited 192 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Enhanced infection of liver sinusoidal endothelial cells in a mouse model of antibody-induced severe dengue disease.

              Raphaël M. Zellweger, Tyler R. Prestwood, Sujan Shresta (2010)
              Dengue virus (DENV) causes disease ranging from dengue fever (DF), a self-limited febrile illness, to the potentially lethal dengue hemorrhagic fever and dengue shock syndrome (DHF/DSS). DHF/DSS usually occurs in patients who have acquired DENV-reactive antibodies prior to infection, either from a previous infection with a heterologous DENV serotype or from an immune mother. Hence, it has been hypothesized that subneutralizing levels of antibodies exacerbate disease, a phenomenon termed antibody-dependent enhancement (ADE). However, given the lack of suitable animal models for DENV infection, the mechanism of ADE and its contribution to pathology remain elusive. Here we demonstrate in mice that DENV-specific antibodies can sufficiently increase severity of disease so that a mostly nonlethal illness becomes a fatal disease resembling human DHF/DSS. Antibodies promote massive infection of liver sinusoidal endothelial cells (LSECs), resulting in increased systemic levels of virus. Thus, a subprotective humoral response may, under some circumstances, have pathological consequences. 2010 Elsevier Inc. All rights reserved.
              Article 0 comments Cited 142 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Journal
                Journal ID (nlm-ta): Front Cell Infect Microbiol
                Journal ID (iso-abbrev): Front Cell Infect Microbiol
                Journal ID (publisher-id): Front. Cell. Infect. Microbiol.
                Title: Frontiers in Cellular and Infection Microbiology
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 2235-2988
                Publication date (Electronic): 21 August 2018
                Publication date Collection: 2018
                Volume: 8
                Electronic Location Identifier: 268
                Affiliations
                [1] 1Department of Dermatology, Kaohsiung Veterans General Hospital , Kaohsiung, Taiwan
                [2] 2Faculty of Yuh-Ing Junior College of Health Care and Management , Kaohsiung, Taiwan
                [3] 3Department of Medical Education and Research, Kaohsiung Veterans General Hospital , Kaohsiung, Taiwan
                [4] 4Department of Medical Laboratory Science and Biotechnology, Chung Hwa University of Medical Technology , Tainan, Taiwan
                Author notes

                Edited by: Alan G. Goodman, Washington State University, United States

                Reviewed by: Akatsuki Saito, Research Institute for Microbial Diseases, Osaka University, Japan; Andrew James Brooks, The University of Queensland, Australia

                *Correspondence: Tsung-Hsien Chang changth@ 123456vghks.gov.tw
                Article
                DOI: 10.3389/fcimb.2018.00268
                PMC ID: 6110916
                PubMed ID: 30186771
                SO-VID: 654584c3-1970-4a01-811f-0f4e33aced0e
                Copyright © Copyright © 2018 Wei, Huang and Chang.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                Date received : 11 April 2018
                Date accepted : 17 July 2018
                Page count
                Figures: 5, Tables: 1, Equations: 0, References: 46, Pages: 10, Words: 6859
                Funding
                Funded by: Ministry of Science and Technology, Taiwan 10.13039/501100004663
                Award ID: MOST 106-2314-B-075B-007 -MY2
                Categories
                Subject: Cellular and Infection Microbiology
                Subject: Original Research

                ScienceOpen disciplines: Infectious disease & Microbiology
                Keywords: dengue virus,hair loss,human hair follicle dermal papilla cells,cell death,inflammation
                Data availability:
                ScienceOpen disciplines: Infectious disease & Microbiology
                Keywords: dengue virus, hair loss, human hair follicle dermal papilla cells, cell death, inflammation

                Comments

                Comment on this article

                scite_

                Similar content426

                See all similar

                Cited by6

                See all cited by

                Most referenced authors657

                See all reference authors