In fact, we regularly observed a 20- to 100-fold-greater level of HIV-1 replication mediated by DCs and B cells compared with direct cis infection of either autologous or heterologous CD4+ T cells, using a relatively low input multiplicity of HIV-1 (m.o.i. 10–3) compared with the 100-fold higher amount of HIV-1 used to demonstrate cis infection (m.o.i. 10–1). The gene discussed is CD4; the disease is infection.