While CD8α antibody administration during chronic infection has been shown in several mmHIV-1 models to result in transient increases in plasma viremia [45,46,53], we have shown that when implemented at the time of infection with the PTM-adapted stHIV-A19 CD8α antibody administration results in an infection course characterized by sustained elevated plasma viral loads, CD4+ T-cell loss, and progression to AIDS-defining clinical diseases [54]. The gene discussed is CD4; the disease is infection.