Dengue virus

About: Dengue virus is a research topic. Over the lifetime, 12671 publications have been published within this topic receiving 461406 citations. The topic is also known as: DENV.

Zika virus, French Polynesia, South Pacific, 2013.

Abstract: To the Editor: We wish to clarify an inaccuracy in a letter in Emerging Infectious Diseases by Cao-Lormeau et al (1) The authors state “In 2007, the first ZIKV outbreak reported outside Africa and Asia was retrospectively documented from biological samples from patients on Yap Island, Federated States of Micronesia, North Pacific, who had received an incorrect diagnosis of dengue virus (DENV)” Although the first outbreak of Zika virus (ZIKV) infection reported outside Africa or Asia was in Yap, it was not retrospectively identified from serum samples incorrectly diagnosed as positive for dengue virus The outbreak was first identified by the Yap State Department of Health Services, and an investigation to determine the etiologic agent was initiated Although dengue was initially part of the differential diagnosis, and a few patients had evidence of IgM against dengue virus by a rapid diagnostic test, clinicians in Yap believed that the clinical syndrome was not consistent with dengue Thus, assistance was requested from the US Centers for Disease Control and Prevention and the World Health Organization to strengthen the epidemiologic investigation and provide confirmatory laboratory testing Serum samples collected during the active investigation were sent to the Arboviral Diseases Diagnostic Laboratory at the Centers for Disease Control and Prevention where testing determined that the cause of the infections was ZIKV (2) This discovery of ZIKV as the etiologic agent was not achieved through retrospective testing of serum from patients incorrectly diagnosed as having dengue, but rather the result of an active, coordinated investigation by the Yap State Department of Health Services with instrumental assistance from international partners

Antibody-enhanced dengue virus infection in primate leukocytes

Abstract: DENGUE viruses, types 1–4, are arthropod-borne flaviviruses which cause dengue shock syndrome (DSS) in humans possessing pre-infection antibody, passively acquired or derived from heterotypic infection1. Although the immuno-pathological mechanism of DSS is not fully understood, experimental studies suggest that dengue virus production is immunologically regulated. Monkeys with monotypic immunity to dengue types 1, 3 or 4 viruses, when challenged with dengue 2, had significantly higher levels of circulating virus than did similarly infected susceptible animals2. This may be attributable to the replication of virus in leukocytes. In infected monkeys, virus was frequently recovered from buffy coat cells and from lymphatic tissues3. The role of leukocytes in enhanced infection is further supported by the observation that dengue replicates readily in cultures of peripheral blood leukocytes (PBL) prepared from immune simian or human donors, but poorly or not at all in leukocytes from non-immune hosts4–6. Studies on the immunological specificity of this phenomenon have been hindered by the requirement either for expensive experimental hosts (monkeys) or for human donors with chronologically defined dengue infections. Here we describe the in vitro enhancement of dengue infection in PBL by antibody. This system provides a provisional model for DSS in young infants during primary dengue infections7,8.

RNA interference screen for human genes associated with West Nile virus infection.

Abstract: West Nile virus (WNV), and related flaviviruses such as tick-borne encephalitis, Japanese encephalitis, yellow fever and dengue viruses, constitute a significant global human health problem. However, our understanding of the molecular interaction of such flaviviruses with mammalian host cells is limited. WNV encodes only 10 proteins, implying that it may use many cellular proteins for infection. WNV enters the cytoplasm through pH-dependent endocytosis, undergoes cycles of translation and replication, assembles progeny virions in association with endoplasmic reticulum, and exits along the secretory pathway. RNA interference (RNAi) presents a powerful forward genetics approach to dissect virus-host cell interactions. Here we report the identification of 305 host proteins that affect WNV infection, using a human-genome-wide RNAi screen. Functional clustering of the genes revealed a complex dependence of this virus on host cell physiology, requiring a wide variety of molecules and cellular pathways for successful infection. We further demonstrate a requirement for the ubiquitin ligase CBLL1 in WNV internalization, a post-entry role for the endoplasmic-reticulum-associated degradation pathway in viral infection, and the monocarboxylic acid transporter MCT4 as a viral replication resistance factor. By extending this study to dengue virus, we show that flaviviruses have both overlapping and unique interaction strategies with host cells. This study provides a comprehensive molecular portrait of WNV-human cell interactions that forms a model for understanding single plus-stranded RNA virus infection, and reveals potential antiviral targets.