2019
DOI: 10.3390/vaccines7010011
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T-Cell Response to Viral Hemorrhagic Fevers

Abstract: Viral hemorrhagic fevers (VHF) are a group of clinically similar diseases that can be caused by enveloped RNA viruses primarily from the families Arenaviridae, Filoviridae, Hantaviridae, and Flaviviridae. Clinically, this group of diseases has in common fever, fatigue, dizziness, muscle aches, and other associated symptoms that can progress to vascular leakage, bleeding and multi-organ failure. Most of these viruses are zoonotic causing asymptomatic infections in the primary host, but in human beings, the infe… Show more

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Cited by 34 publications
(37 citation statements)
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References 249 publications
(345 reference statements)
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“…The role of T cells in viral hemorrhagic fevers has not been characterized and the protective or pathogenic contribution of T cells is unclear (37). However, the protective role of memory CD8 cells presenting cross-reactive epitopes has been shown to protect against secondary DENV infections in endemic areas (38,39).…”
Section: Discussionmentioning
confidence: 99%
“…The role of T cells in viral hemorrhagic fevers has not been characterized and the protective or pathogenic contribution of T cells is unclear (37). However, the protective role of memory CD8 cells presenting cross-reactive epitopes has been shown to protect against secondary DENV infections in endemic areas (38,39).…”
Section: Discussionmentioning
confidence: 99%
“…While vaccines are being developed, dose-sparing methods are being investigated [121,122]. One method, intradermal administration of YF vaccine, mimics the natural route of transmission and takes advantage of the skin dendritic cells role in the immune response [123,124]. In one study, the immunogenicity of a fractional (one-fifth) intradermal dose of YF 17D vaccine was not inferior to that of a full subcutaneous dose.…”
Section: Yellow Fever Vaccine Candidatesmentioning
confidence: 99%
“…Additionally, innate and adaptive (humoral and cellular) immune responses were shown to be activated during the infection (reviewed in [ 15 ]). The infection results in the activation of type-I effector mechanisms (cytotoxicity and interferon production) as well as strong T cell activation and differentiation (reviewed in [ 16 ]). Similar results were obtained using non-human primates (NHP) model, the ‘gold-standard’ animal model of EBOV infection, (reviewed in [ 17 , 18 ]) confirming the role of the immune response in pathogenesis of the disease.…”
Section: Introductionmentioning
confidence: 99%