Response to Bandera et al.

To the Editor—We thank Bandera et al for their interesting exploration of the relationship between innate immune activation phenotypes and the failure of immunologic reconstitution after initiation of antiretroviral therapy (ART), in response to our published findings [1]. They demonstrate an intriguing association between immunologic nonresponse (INR, CD4 < 350 cells/µL) and increased frequency of cellular markers of innate immune activation, particularly higher levels of intermediate (CD14++CD16+) monocytes, lower expression of CD163 on total and classical (CD14++CD16−) monocytes, and a higher proportion of intermediate monocytes expressing CD11b, all of which support a shift of monocyte phenotype away from classical monocytes and toward intermediate and nonclassical monocyte subtypes. Although their comparisons are unadjusted and the observed differences are small, their investigation is one of the first to examine the role of innate immune activation, and monocytes in particular, in INR.