ICAM-1 levels have previously been associated with increased productive infection of CD4+ T cells,20 and with inflammatory responses and HIV disease progression.41 Furthermore, upregulation of ICAM-1 promotes HIV-mediated syncytia formation and viral spread.21–23 These mechanisms, alone or in combination, could explain the increased ability of HA-deficient fibroblasts to augment HIV infection of T cells. The gene discussed is CD4; the disease is HIV infectious disease.