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TO THE EDITOR—With great interest we read the recent study by Boudová et al [1] who investigated the impact of chronic human immunodeficiency virus (HIV) infection on the frequency and differentiation status of CD4 Vγ2Vδ2 T cells in peripheral blood of patients from an African American cohort with a focus on patients with slow disease progression and low viral loads. These patients were termed " persistently viremic " (PV) by the authors, which is a less stringent definition of the more commonly used phrase " long-term nonprogressors " [2]. Boudová et al describe in this study how Vγ2Vδ2 cells are severely altered with regard to memory phenotype and expression of the cytotoxicity marker CD56 in HIV-infected patients [1]. We performed a similar analysis in a cohort consisting predominantly of white individuals, classified as healthy donors (HDs), antiretroviral therapy (ART)– treated HIV patients (HAARTs), and elite controllers (ECs), as shown in Figure 1A. In addition, we added a group of PV HIV patients, according to the definition of Boudová et al [1] for reasons of direct comparability, as well as patients with a viral load >100 000 copies/mL (HV) who were not included in the previous report [1]. Written informed consent was obtained from all patients and the study was approved by the local ethics committee. Vγ2Vδ2 T cells were defined as CD3+TCRgd+Vδ2+ lympho-cytes, as shown in Figure 1B. All samples were run on an LSR II flow cytometer (BD) and analyzed with FlowJo Version 9 diagnostic software. We also found alterations in the CD4 Vγ2Vδ2 T cell compartment in HIV patients , albeit with noteworthy differences. In agreement with a previous report [3], there was a trend toward a decreased frequency of Vγ2Vδ2 T cells among lym-phocytes from HIV-infected individuals compared to HDs (Figure 1C). However, in our viremic (HV and PV) patients, but not in HAARTs or in ECs, we saw a significant skewing of the Vγ2Vδ2 subset toward an activated (CD38+Ki67+, data not shown) and terminally differentiated (CCR5−/CD28−) effector phenotype compared to HDs (Figure 1D). This is in stark contrast to the results of Boudová et al, who describe a trend toward a decline of the proportion of T effector memory (CD27−CD45RA−) cells in the Vγ2Vδ2 T cell compartment in all HIV-positive groups. We confirmed our results by additional memory marker staining for CD27−CD28− cells (data not shown). In general, accumulations of terminally differentiated and activated/ exhausted T …

Vγ2Vδ2 T Cells are Skewed Toward a Terminal Differentiation Phenotype in Untreated HIV Infection