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dc.creatorGarjito, Triwibowo Ambar; Balai Litbang P2B2 Donggala
dc.descriptionDengue hemorrhagic fever is still one of the major public health problem worldwide, particularly in sub tropical and tropical regions. The disease is caused by the presence of dengue virus infection (DENVa), member of the Flaviviridae family. Dengue virus is composed by three structural proteins (C, M, E) and seven non-structural proteins. Organization of the dengue virus genome is 5'-UTR-C-prM-E-NS1-NS2A-NS2B-NS3-NS4A-NS4B-NS5-UTR-3' (UTR-: untranslated region; C; Capsid; PrM: Precursor membrane; E: Envelope; NS: non-structural). Dengue virus will be able to bind with the hospes cell through two ways, a. Virus bound to the receptors on the cell surface via anti-dengue antibodies that bound to the cell. Onca attached, the virus entry into the cell in to ways, namely endocytosis/pinocytosis, and b. Fusion between the viral envelope with the plasma membrane followed release of the nuclecapsid into the cytoplasm of cells. Dengue virus can causing illness through infecting and killing these cells, or through stimulation of host immune response that will cause the cells to be induced. Pathogenesis studies have also shown that the most patients with DHF are caused by secondary infections. Studies have been conducted in chimpanzees showed that the dengue virus serum titer was higher during secondary infection that during primary infection. During the occurance of secondary infection by a heterologous serotype of dengue virus, antibodies can recognize the virus and bind to form virus-antibody compleexs. The complex will easier enter into the host cell rather than that is encapsuled via mononuclear cells that have Fcy receptors, especially macrofag. In addition, cross-reactive antibodies fail to neutralize the virus, so the virus will replicate in the other free cells. This phenomena is known as antibody dependent enhancement (ADE).en-US
dc.publisherBalai Penelitian dan Pengembangan Pengendalian Penyakit Bersumber Binatang Donggalaen-US
dc.rightsPublishing your paper with Jurnal Vektor Penyakit (JVP) means that the author or authors transfer the copyright to JVP. JVP granted an exclusive reuse license by the author(s), but the author(s) are able to put the paper onto a website, distribute it to colleagues, give it to students, use it in your thesis etc, even commercially. JVP journal provides immediate open access to its content on the principle that making research freely available to the public supports a greater global exchange of knowledge. This journal is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License. This license lets others remix, transform, and build upon the material for any purpose, even commercially. JVP journal Open Access articles are distributed under this Creative Commons Attribution-ShareAlike 4.0 International License (CC BY-SA). Articles can be read and shared for All purposes under the following conditions: BY: You must give appropriate credit, provide a link to the license, and indicate if changes were made. You may do so in any reasonable manner, but not in any way that suggests the licensor endorses you or your use. SA: If you remix, transform, or build upon the material, you must distribute your contributions under the same license as the original.  Download Copyright Transfer Form
dc.sourceJurnal Vektor Penyakit; Vol 5, No 1 (2011); 54-63id-ID
dc.sourceJurnal Vektor Penyakit; Vol 5, No 1 (2011); 54-63en-US
dc.subjectvirus dengue, molekuler dengue, imunopathogenesisen-US
dc.titleVirus Dengue: Dasar Molekuler, Mekanisme Masuknya ke dalam Sel Target serta Imunopathogenesis yang Ditimbulkannyaen-US
dc.typePeer-reviewed Articleen-US

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