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Background Postnatal transmission via breastfeeding is a leading cause of infant HIV infection in the developing world. However, only a small minority of breastfed infants born to HIVinfected women become infected. As a genetic bottleneck severely restricts the number of postnatally-transmitted variants, genetic or phenotypic differences in the virus Envelope (Env) may play a role in its ability to breech the mucosal barrier in the infant gastrointestinal tract.

Postnatally-transmitted HIV-1 variants are efficient at dendritic cell trans-infection and sensitive to autologous and heterologous neutralization