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OBJECTIVES: People with HIV (PWH) are at increased risk for premature cardiovascular disease (CVD). Clonal hematopoiesis is a common age-related condition that may be associated with increased CVD risk. The goal of this study was to determine the prevalence of clonal hematopoiesis and its association with chronic inflammation and CVD in PWH. DESIGN: Cross-sectional study utilizing archived specimens and data from 118 men (86 PWH and 32 HIV-uninfected) from the Baltimore-Washington DC center of the Multicenter AIDS Cohort Study (MACS) who had had coronary computed tomography angiography (CTA) and measurement of 34 serologic inflammatory biomarkers. METHODS: Clonal hematopoiesis was assessed on peripheral blood mononuclear cells utilizing targeted error-corrected next generation sequencing (NGS) focused on 92 genes frequently mutated in hematologic malignancies. Clinical and laboratory data were obtained from the MACS database. RESULTS: Clonal hematopoiesis with a variant allele frequency (VAF) greater than 1% was significantly more common in PWH [20/86 (23.3%)] than in HIV-uninfected men [2/32 (6.3%)] (P = 0.035). PWH with clonal hematopoiesis (VAF > 1%) were more likely to have coronary artery stenosis of at least 50% than those without clonal hematopoiesis [6/20 (30%) vs. 6/64 (9%); P = 0.021]. Presence of clonal hematopoiesis was not significantly associated with serological inflammatory markers, except for significantly lower serum leptin levels; this was not significant after adjustment for abdominal or thigh subcutaneous fat area. CONCLUSION: Clonal hematopoiesis was more common in PWH and among PWH was associated with the extent of coronary artery disease. Larger studies are needed to further examine the biological and clinical consequences of clonal hematopoiesis in PWH.

We studied viral evolution in five human leukocyte antigen (HLA)-B*57 patients recently infected with HIV-1. Escape mutations in HLA-B*57-restricted Gag epitopes were present at study entry in all patients, but were not associated with significant increases in viremia. Conversely, no new escape mutations in HLA-B*57-restricted epitopes or known compensatory mutations were detected in patients who experienced significant increases in viremia. Thus, the development of escape mutations alone does not determine virologic outcome in recently infected HLA-B*57 patients.

Interleukin (IL)-2 has been studied as a treatment for HIV infection because it stimulates the proliferation of T cells and augments antiviral immune functions [1,2]. Two regimens have been used: intermittent IL-2 (5 days every 8 weeks, usually 4.5–9 million international units (mIU)/day) and ultra-low-dose (ULD) IL-2 (1.2 mIU/m2/day), which can be given daily for weeks or months [1]. In patients with chronic and early/acute HIV infection, neither regimen has conferred any health benefit when given with concurrent antiretroviral therapy (ART) [3–7], and in patients with chronic HIV infection, ULD IL-2 did not improve viral control after stopping ART [8]. However, treatment of acute/early HIV infection with daily ULD IL-2 and interruption of ART has not been studied. We treated one patient who had taken ART since 1 month after HIV seroconversion with daily ULD IL-2. After receiving IL-2, this patient’s viral load set point off highly active antiretroviral therapy (HAART) was less than 50 copies/ml as compared with 39 000 copies/ml when ART was stopped without IL-2. Further, after IL-2 was stopped, viral load did not rebound for 14 months without ART. A 29-year-old man tested HIV-positive by ELISA and western blot 1.5 months after a negative ELISA, and was treated 30 days later with zidovudine, lamivudine, and efavirenz. Viral load was undetectable for 4 years on ART (with minor changes in regimen), except for occasional blips (all