We found that after ex vivo infection of unstimulated PBMCs, infected cells concomitantly upregulated the expression of CD32 and the activation marker HLA-DR; productively infected cells expressing HIV RNA and Gag protein upregulated both markers to a greater degree (2-fold increase) than cells transcribing only HIV RNA (1.5-fold increase). The gene discussed is FCGR2A; the disease is infection.