| Journal: | Salus |
| Database: | PERIÓDICA |
| System number: | 000342918 |
| ISSN: | 1316-7138 |
| Authors: | Bosch, Irene1 Muñoz Jordán, Jorge L |
| Institutions: | 1University of Massachusetts, Medical School, Worcester, Massachusetts. Estados Unidos de América 2Centers for Disease Control and Prevention, Division of Vector Borne Infectious Diseases, San Juan. Puerto Rico |
| Year: | 2008-2009 |
| Volumen: | 12 |
| Pages: | 35-42 |
| Country: | Venezuela |
| Language: | Inglés |
| Document type: | Artículo |
| Approach: | Analítico |
| Spanish abstract | mecanismos moleculares de la patogénesis viral y determinarán mejoras en el diagnóstico y la terapia |
| English abstract | Dengue virus (DENV) produces a wide range of illness, going from asymptoBmatic infections to hemorrhagic disease. This mosquito-borne flavivirus causes about 50 million infections annually (mainly in the tropics), most them resulting in a febrile illness. Dengue hemorrhagic fever (potentially fatal vascular leakage syndrome), appears less frequently. The innate immune response of the host plays an important role during the initial stages of infection. Severe disease is associated with high viremias, immune enhancement of sequential infections and exacerbated inflammatory response. DENV is sensed in mammalian cells by endosomal and cytoplasmic receptors and stimulates the host innate immune response, in particular the type-1 interferon (IFN α/β) response which acts on target cells by stimulating the JAK/STAT signaling network. This results in activation of genes that lead the infected cells toward an antiviral response. Genomic technology allowed the identification of human genes induced in response to DENV. The results define common antiviral and pro-inflammatory responses composed mainly of IFN α/β induced genes, which likely participate in the regulation of the immune response and induce vascular leakage during the acute phase of the disease. DENV can also circumvent the IFN α/β response of the host. Apparently, non-structural proteins of DENV weaken IFN α/β signaling, causing reduced response in activation of gene expression. Increased virus uptake, weakening of the host cell defense, and unrestrained inflammatory response likely predispose patients to develop severe illness. The identification of antiviral response signature genes and the discovery of crucial virus-host interactions lead to a better understanding of the molecular mechanisms of viral pathogenesis and will serve to improve diagnosis and therapy |
| Disciplines: | Medicina, Biología |
| Keyword: | Microbiología, Inmunología, Virus, Virus del dengue, Interferón, Hospederos, Señalización, Respuesta inflamatoria |
| Keyword: | Medicine, Biology, Microbiology, Immunology, Virus, Dengue virus, Interferon, Hosts, Signaling, Inflammatory response |
| Full text: | Texto completo (Ver PDF) |
