Publications by authors named "Bryan Castillo-Rojas"
Article Synopsis
- - Flaviviruses are a group of viruses that cause serious diseases in humans, including dengue and Zika, and rely on a protein called NS1 for replication and disease severity.
- - NS1 is secreted from infected cells and contributes to endothelial dysfunction, which affects blood vessel permeability and may facilitate the spread of the virus in the body.
- - Research demonstrates that NS1 aids in the virus's ability to cross endothelial barriers and boosts the infectivity of specific target cells, indicating its crucial role in virus dissemination and its impact on disease progression.
Dengue virus (DENV) is a medically important flavivirus causing an estimated 50-100 million dengue cases annually, some of whom progress to severe disease. DENV non-structural protein 1 (NS1) is secreted from infected cells and has been implicated as a major driver of dengue pathogenesis by inducing endothelial barrier dysfunction. However, less is known about how DENV NS1 interacts with immune cells and what role these interactions play.
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- * DENV NS1 activates inflammasomes in macrophages, leading to the release of IL-1β, but this process does not result in cell death, allowing macrophages to survive while responding to the virus.
- * Research shows that the inflammasome pathway, particularly involving caspase-1, is crucial for immune response, as mice lacking this pathway are more vulnerable to severe DENV infections.
Severe COVID-19 is associated with epithelial and endothelial barrier dysfunction within the lung as well as in distal organs. While it is appreciated that an exaggerated inflammatory response is associated with barrier dysfunction, the triggers of vascular leak are unclear. Here, we report that cell-intrinsic interactions between the Spike (S) glycoprotein of SARS-CoV-2 and epithelial/endothelial cells are sufficient to induce barrier dysfunction in vitro and vascular leak in vivo, independently of viral replication and the ACE2 receptor.
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