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Henry Puerta-Guardo

Researcher at University of California, Berkeley

Publications -  40
Citations -  2214

Henry Puerta-Guardo is an academic researcher from University of California, Berkeley. The author has contributed to research in topics: Dengue virus & Dengue fever. The author has an hindex of 18, co-authored 31 publications receiving 1627 citations. Previous affiliations of Henry Puerta-Guardo include Instituto Politécnico Nacional & Universidad Autónoma de Yucatán.

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Zika Virus Targets Different Primary Human Placental Cells, Suggesting Two Routes for Vertical Transmission.

TL;DR: It is suggested that ZIKV spreads from basal and parietal decidua to chorionic villi and amniochorionic membranes and that targeting TIM1 could suppress infection at the uterine-placental interface.
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Dengue virus NS1 triggers endothelial permeability and vascular leak that is prevented by NS1 vaccination

TL;DR: The results of in vitro and in vivo experiments point to circulating dengue virus non-structural protein 1 (NS1) and the innate immune Toll-like receptor 4 (TLR4) as a focus for basic scientists as well as vaccine and drug developers.
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Dengue Virus NS1 Disrupts the Endothelial Glycocalyx, Leading to Hyperpermeability.

TL;DR: It is demonstrated that DENV NS1 disrupts the EGL on human pulmonary microvascular endothelial cells, inducing degradation of sialic acid and shedding of heparan sulfate proteoglycans, which suggests an important role for EGL disruption in DENVNS1-mediated endothelial dysfunction during severe dengue disease.
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Flavivirus NS1 Triggers Tissue-Specific Vascular Endothelial Dysfunction Reflecting Disease Tropism

TL;DR: It is demonstrated that NS1 from dengue, Zika, West Nile, Japanese encephalitis, and yellow fever viruses selectively binds to and alters permeability of human endothelial cells from lung, dermis, umbilical vein, brain, and liver in vitro and causes tissue-specific vascular leakage in mice, reflecting the pathophysiology of each flavivirus.
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Dengue virus NS1 cytokine-independent vascular leak is dependent on endothelial glycocalyx components

TL;DR: Data indicate that DENV NS1-induced endothelial cell-intrinsic vascular leak is independent of inflammatory cytokines but dependent on endothelial glycocalyx components.