Additionally in 2004, Jindadamrongwech and Smith identified the 78kDa band for DENV2 as the glucose-related protein, GRP78 (BiP) on membrane extracts of HepG2 [48]. Pretreatment with anti-GRP78 antibodies resulted in a partial inhibition of DENV2 infection suggesting that additional receptor elements were involved in the entry process of DENV. In 2007, Cabrera-Hernandez and coworkers again noted a modest but definite inhibition of DENV2 entry into HepG2 cells in the presence of specific antibody directed against GRP78 [49]. The reproducible inhibition about 40% of the viral wild-type entry clearly demonstrated that GRP78 acted as at least a minor receptor in DENV internalization [49]. Moreover, it was reported that liver/lymph node-specific ICAM-3-grabbing integrin (L-SIGN) [50], homolog of DC-SIGN, expressed on liver sinusoidal endothelial cells as well as a subset of endothelial cells in the paracortex zone of lymph nodes, had the ability to bind to DENVs [51, 52]. And its expression in THP-1 cells induced susceptibility to DENV infection [53]. Specific antibodies against L-SIGN could subsequently block the acquired susceptibility. The L-SIGN-dependent DENV infection of THP-1 cells offered an intriguing possibility for the participation of L-SIGN in DENV infection [49].6. Fc ReceptorsGenerally, DENV infection can induce subtype-specific humoral and cellular immune responses. If a secondary infection is caused by another serotype of DENV in the same individual, the preexisting antibodies will mediate virus infecting monocytes more efficiently. The outcome may be an increase in the viral replication and a high risk of severe dengue. This situation is referred to as antibody-dependent enhancement (ADE) of DENV infection. One possibility explaining this phenomenon is that in secondary infections, the virus may enter cells through the primary receptor(s) or it may also form immune complexes with preexisting nonneutralizing antibodies and interact with an alternative receptor, such as the immunoglobulin G (IgG) receptor (Fc gamma receptor, Fc��R), which exists in Fc��R-bearing cells including monocytes/ macrophages [54, 55]. By this process, the antibody-virus complexes may increase the ability of the virus to bind to and internalize into host cells, leading to maximum productive infection, that is, ADE of infection.7. DENV Receptors on Mosquito Cells Generally more is known about the detail of DENV replication cycle in mammalian cells as compared with that in mosquito cells. An Aedes albopictus mosquito cell line (C6/36) was frequently used for almost all studies associated with DENV receptors in host of mosquito during recent years.