In the past few years, many studies revealed that host immunogenetics, including genetic polymorphisms, play important roles in host resistance to HIV-1 infection and predict different progressions to AIDS after infection [5] [6] [7] . Polymorphisms of certain chemokines and chemokine receptors have been reported to play important roles in individual variability in response to HIV-1/AIDS. The most investigated variation is the 32-bp deletion in the chemokine receptor-5 (CCR5 D32) gene, which was shown to confer resistance to HIV-1 infection in homozygous carriers, and its role has been investigated in a clinical context [8, 9] . Similar to CCR5, DC-SIGNR is potentially an important gene affecting host susceptibility to HIV-1 infection and disease progression. DC-SIGN (dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin) is able to bind the HIV-1 gp120 surface glycoprotein with high affinity and is able to enhance trans-infection of T cells by HIV-1 [10] . DC-SIGNR is a homolog of DC-SIGN with 77% amino acid identity and preferential expression in liver and lymph node epithelial cells. DC-SIGNR functions similarly to DC-SIGN in capturing HIV-1 and enhancing HIV-1 infection of T cells [11] .