The interesting finding that the SF162- but not LAI-infected fraction had a significantly higher percentage of IFN-γ+ and MIP-1β+ T-cells than the total population (Fig 3E) led us to speculate that SF162 (R5) infection resulted in upregulation of these cytokines through CCR5 engagement rather than the specific cell phenotype being targeted by SF162 (R5) virus. The gene discussed is CCR5; the disease is infection.