Dengue 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).