S. Moses DennisonKara M. AnastiFrederick H. JaegerShelley M. StewartJustin PollaraPinghuang LiuErika L. KunzRuijun ZhangNathan VandergriftSallie PermarGuido FerrariGeorgia D. TomarasMattia BonsignoriNelson L. MichaelJerome H. KimJaranit KaewkungwalSorachai NitayaphanPunnee PitisuttithumSupachai Rerks-NgarmHua Xin LiaoBarton F. HaynesS. Munir AlamDuke University School of MedicineWalter Reed Army Institute of ResearchMahidol UniversityArmed Forces Research Institute of Medical Sciences, ThailandThailand Ministry of Public Health2018-11-092018-11-092014-01-01Journal of Virology. Vol.88, No.16 (2014), 9406-9417109855140022538X2-s2.0-84904878889https://repository.li.mahidol.ac.th/handle/20.500.14594/34052Mucosal epithelial cell surface galactosylceramide (Galcer) has been postulated to be a receptor for HIV-1 envelope (Env) interactions with mucosal epithelial cells. Disruption of the HIV-1 Env interaction with such alternate receptors could be one strategy to prevent HIV-1 entry through the mucosal barrier. To study antibody modulation of HIV-1 Env-Galcer interactions, we used Galcer-containing liposomes to assess whether natural- and vaccine-induced monoclonal antibodies can block HIV-1 Env binding to Galcer. HIV-1 Env gp140 proteins bound to Galcer liposomes with KdS (dissociation constants) in the nanomolar range. Several HIV-1 ALVAC/AIDSVAX vaccinee-derived monoclonal antibodies (MAbs) specific for the gp120 first constant (C1) region blocked Galcer binding of a transmitted/founder HIV-1 Env gp140. Among the C1- specific MAbs that showed Galcer blocking, the antibody-dependent cellular cytotoxicity-mediating CH38 IgG and its natural IgA isotype were the most potent blocking antibodies. C1-specific IgG monoclonal antibodies that blocked Env binding to Galcer induced upregulation of the gp120 CD4-inducible (CD4i) epitope bound by MAb 17B, demonstrating that a conformational change in gp120 may be required for Galcer blocking. However, the MAb 17B itself did not block Env-Galcer binding, suggesting that the C1 antibody-induced gp120 conformational changes resulted in alteration in a Galcer binding site distant from the CD4i 17B MAb binding site. © 2014, American Society for Microbiology.Mahidol UniversityImmunology and MicrobiologyArticleSCOPUS10.1128/JVI.01031-14