patient. 1 The potential second case of the Mississippi baby brought additional excite- ment; however, the re‐emergence of virus in this infant has given pause to hopes for additional functional cures. 2 At the recent IAS conference on HIV/AIDS, Zaunders et al 3 presented on patient C135, one of the delta nef deleted HIV virus recipients in the Sydney blood bank cohort, who is not on antiretroviral medications and in whom infectious virus cannot now be detected. Whether this person is functionally cured or in remission is unknown. C135 has some genetic biomarkers that are associ- ated with slower disease progression: HLA‐B*57 positivity and heterozygosity for the CCR5Delta 32 mutation. As HIV researchers develop strategies for regimens designed toward functional cure, we pro- pose that in HIV-infected persons in whom functional cure regimens are being consid- ered, and in whom therapeutic vaccination is a proposed intervention, immunogenom- ic approaches are taken into account to prioritize initial studies. For example, those with HLA or KIR alleles associated with slow progression, such as HLA‐B*57, 4 Delta 32CCR5 heterozygosity, 5 overex- pression of intrinsic resistance genes, 6 and others, could be candidates prioritized for these studies. We call this identification of “remission ready” patients. Oncologists stage patients based on a number of biomarkers for entry into differential clin- ical practices. HIV health practitioners enrolling subjects into functional cure regimens that include therapeutic immuni- zations should consider taking immunoge- nomics into account when identifying remission ready patients. Although the ultimate goal for HIV research is a universal cure and effective vaccine, this Sydney blood bank cohort subject has shown that genetics is a pow- erful indicator of viral suppression and potential remission. Immunogenomic pro- filing can help identify other such “remis- sion ready patients.” This strategy could be described as “test” (immunogenomic profiling), “treat” (provide antiretroviral therapy), and “cure” (augmentative thera- pies designed for functional cures). ACKNOWLEDGMENTS The authors thank the District of Columbia Developmental Center for AIDS Research (P30AI087714). Douglas F. Nixon, MD, PhD* Gary L. Simon, MD† Rui André Saraiva Raposo, PhD* *Department of Microbiology, Immunology & Tropical Medicine, The George Washington University, Washington, DC †Division of Infectious Diseases, Department of Medicine, The George Washington University, Washington, DC REFERENCES 1. Hutter G, Nowak D, Mossner M, et al. Long‐ term control of HIV by CCR5 Delta32/Delta32 stem‐ cell transplantation. N Engl J Med. 2009;360:692– 698. 2. Ledford H. HIV rebound dashes hope of “Mississippi baby” cure. Nat News. July 10, 2014. doi:10.1038/nature.2014.15535. 3. Zaunders J, Dyer WB, Churchill M, et al. Possible clearance of transfusion‐acquired nef‐deleted attenuated HIV‐1 infection by a long‐term non‐ progressor with CCR5 Delta32 heterozygous and HLA‐B57/DR13 genotype. Presented at: AIDS 2014, 20th International AIDS Conference, Mel- bourne, Australia, July 20–25, 2014. Abstract TUAA0105. 4. Pereyra F, Jia X, McLaren PJ, et al. The major genetic determinants of HIV‐1 control affect HLA class I peptide presentation. Science. 2010;330:1551–1557. 5. Huang Y, Paxton WA, Wolinsky SM, et al. The role of a mutant CCR5 allele in HIV‐1 trans- mission and disease progression. Nat Med. 1996;2:1240–1243. 6. Raposo RA, Abdel‐Mohsen M, Holditch SJ, et al. Increased expression of intrinsic antiviral genes in HLA‐B*57‐positive individuals. J Leukoc Biol. 2013;94:1051–1059. Evaluation of the Efficacy and Safety of Switching to Tenofovir, Emtricitabine, and Rilpivirine in Treatment- Experienced Patients To the Editors: Rilpivirine (RPV), a recently licensed nonnucleoside reverse tran- scriptase inhibitor, has shown noninfe- rior efficacy and a favorable safety profile compared with efavirenz (EFV) in treatment-naive HIV-1–infected adults. 1,2 In the SPIRIT study, noninferior efficacy has also been observed among patients who switched to an RPV-containing versus protease inhibitor (PI)-containing antiretroviral (ARV) regimen. 3 Switching from tenofovir (TDF)/emtricitabine (FTC)/EFV to TDF/FTC/RPV was also shown to be a safe and efficacious option for 49 virologically suppressed HIV- infected patients. 4 To date, there has been no confirmation of the results from this trial in real-world settings. Moreover, changes in residual viremia at ultralow detection levels, which could potentially predict virologic failure, 5 have never been evaluated after switching to an RPV-containing ARV regimen. The objective of our study was then (1) to assess efficacy and safety of switching to TDF/FTC/RPV among patients whose HIV was already suppressed (below 20 copies/mL) and (2) to determine whether rates of ultrasensitive HIV detec- tion shed light on the efficacy of this treatment strategy. We conducted a prospective study at Saint-Antoine Hospital (Paris, France). From September 2012 to May 2013, all patients with plasma HIV-RNA ,20 copies per milliliter switching to TDF/ FTC/RPV were consecutively included. Clinical and biological (immunological, virological, liver function, lipids) data were collected at baseline, month-3 (M3), and month-6 (M6). In a subset of patients, ultrasensitive viral loads (US-VL) were measured in plasma by an adapted Cobas/TaqmanHIV-1ultrasensitive assay (quantification limit ,1 copy/mL) before and after switching ARV regimens. Viro- logic failure was defined as 2 consecutive HIV-RNA .20 copies per milliliter. Sequences of protease and reverse tran- scriptase genes on RNA or DNA at baseline and at the time of virologic failure were determined using ANRS consensus- technique primer sequences, as described at http://www.hivfrenchresistance.org. Statistical analyses were performed with STATA12.1 (College Station, TX), and significance was determined using a P value of ,0.05. Signed informed consent to use biomedical data for medical research was obtained from all patients. Presented at Journées Nationales d’Infectiologie Meet- ing, June 12–14, 2013, Clermont-Ferrand, France. The authors have no funding or conflicts of interest to disclose. Letters to the Editor J Acquir Immune Defic Syndr  Volume 68, Number 1, January 1, 2015 e10 | www.jaids.com Ó 2014 Lippincott Williams & Wilkins