Dengue virus (DENV) is the causative agent of dengue fever and the more severe forms of the infection known as dengue haemorrhagic fever and dengue shock syndrome (DHF/DSS). Secondary infections with a serotype different from the primary infection are considered a risk factor for the development of DHF/DSS. One explanation for the increased risk of DHF/DSS development after heterologous secondary infections is the antibody-dependent enhancement (ADE) hypothesis. This hypothesis postulates that pre-existing non-neutralizing antibodies will form immune complexes with the new serotype-infecting virus that in turn will have enhanced capacity to infect macrophages and other Fcgamma receptor (FcgammaR)-bearing cells. Despite the evidence supporting the ADE hypothesis, the molecular mechanisms of ADE are not fully understood. In this work, we present evidence which indicates that intact lipid rafts are required for the ADE infection of U937 cells with DENV. Flow cytometry analysis to measure the percentage of infected cells showed that treatment of differentiated U937 cells with nystatin (30 microg ml(-1)), filipin (10 microg ml(-1)) or beta-methyl cyclodextrin (30 mM) significantly reduces (P<0.05) the ADE of DENV-4 infection in vitro without any effect on viability or the number of FcgammaR-bearing cells. Later cholesterol replenishment by supplementing treated cell cultures with bovine fetal serum for 24 h re-established lipid raft integrity and reversed the alteration of the ADE in vitro (P<0.05). Our results suggest that ADE of U937 infection by DENV requires the presence of cholesterol and cholesterol-rich membrane microdomains.

Antibody-dependent enhancement of dengue virus infection in U937 cells requires cholesterol-rich membrane microdomains.

Dengue fever is a major tropical infectious disease that affects 50-100 million people each year. Its complications, namely dengue haemorrhagic fever and dengue shock syndrome, disproportionately afflict children and young adults. The primary goal of several vaccines now in development is to elicit protective neutralizing antibody responses; however, the exact definition of such responses remain unclear. Here, we review briefly the historical aspects of dengue vaccine development and current candidate dengue vaccines, and discuss various laboratory assays for gauging the neutralizing antibody responses to infection or vaccination, or both. We conclude that modification of current neutralization assays is required to improve the correlation between neutralization end point determinations and protection against secondary heterotypic dengue infections.

https://www.intmedpress.com/serveFile.cfm?sUID=c72f99af-7c47-44e8-8dd1-82564441f868

Dengue vaccine development and dengue viral neutralization and enhancement assays.

The present study analyzes the importance of the inflammasome that involves the NLRP3 complex in the state of hypercytokinemia observed in patients with COVID-19, significantly increasing IL-1β, IL18, IL-6, and TNF. Unfortunately, improving the immune response can sometimes worsen the outcome of the disease. Studies show that colchicine, among other actions, inhibits the assembly of NLRP3 complex that is responsible for generating the active form of Caspase-1 that will convert Pro-IL-1β and Pro-IL-18 into their active forms. We suggest using colchicine, a class of drugs with low-cost, extensively tested, well-tolerated medicine as a complementary treatment for patients with COVID-19, in early stages of the disease based on knowledge of its immunomodulatory properties.

The therapeutic potential of colchicine in the complications of COVID19. Could the immunometabolic properties of an old and cheap drug help

Dengue virus (DV) infections are a serious cause of morbidity and mortality in most tropical and subtropical areas of the world. Dengue virus infection can be asymptomatic or causes two forms of illness, dengue fever (DF) and dengue hemorrhagic fever (DHF), which is the severe form of dengue illness and often fatal. In subsequent infection with a dengue virus of different serotype, severe disease is linked to high levels of antibody-enhanced viral replication early in illness which is followed by a cascade of memory T-cell activation, other cells of immune system and a production of inflammatory cytokines and other chemical mediators that cause an increase in vascular permeability. Advances in that field of immunology have shown that DHF/DSS pathogenesis is a complex, multifactorial process related with host and viral factors that influence disease severity.

/pdf/papel-del-sistema-inmune-en-la-patogenia-de-la-infeccion-por-2n1l8w3kiv.pdf

Papel del sistema inmune en la patogenia de la infección por el virus del dengue

Dengue virus (DENV) is a critical public health concern in tropical and subtropical regions worldwide. Thus, immunocompetent murine models of DENV infection with robust viremia are required for vaccine studies. Diabetes is highly prevalent worldwide, making it frequent comorbidity in patients with dengue fever. Therefore, murine models are needed to understand viral pathogenesis and disease progression. Acquired‐induced and inherently diabetic C57BL/6 and db/db mice were inoculated with DENV‐3 via the tail vein. After infection, both the diabetic C57BL/6 and db/db mice showed obvious weight loss with clinical manifestations. Quantitative reverse‐transcription polymerase chain reaction revealed robust and replicable viremia in the two types of diabetic mice. Immunohistochemical detection showed persistent DENV‐3 infection in the liver. Enzyme‐linked immunosorbent assay for cytokine detection revealed that diabetic mice showed more severe inflammatory responses than did nondiabetic mice, and significant histological alterations were observed in diabetic mice. Thus, the diabetic mice were more susceptible to DENV infection than the nondiabetic mice. Taken together, we established two types of immunocompetent diabetic mice for DENV infection, which can be used to further study the mechanisms of dengue pathogenesis in diabetes and to develop antiviral pharmaceuticals and treatments.

Murine diabetic models for dengue virus infection

Dengue fever is gaining increased attention as a major global health problem. It occurs annually in 50–100 million people in more than 100 countries, and places half a million people at risk of life-threatening diseases: dengue hemorrhagic fever and dengue shock syndrome (DHF/DSS). The pathogenic mechanisms causing DHF/DSS are not clearly understood. This article reviews cellular and molecular mechanisms that might be responsible for the initiation of the pathogenic processes, including hypotheses for DHF/DSS, dengue-permissive target cells, putative dengue receptors, neutralizing and enhancing antibodies to dengue virus, mechanisms of vascular plasma leakage, innate immune response in dengue infection and antibody-dependent enhancement of dengue infection. While reviewing the literature, the article also gives the author’s opinion on perceived areas of importance for future research in human dengue pathogenesis.

Cellular and molecular basis of antibody-dependent enhancement in human dengue pathogenesis

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Cellular and molecular basis of antibody-dependent enhancement in human dengue pathogenesis