LILRA4 and HIV infectious disease: Second, a potential difference in the efficiency of virus transmission from infected T cell to pDCs cannot explain why depletion of ILT7 in pDCs eliminates the modulatory effect of Vpu on IFN-I production nor why a differential activation of ILT7 by WT or dU HIV-expressing cells can be observed with a reporter cell line that is not susceptible to HIV infection (Fig 9).