Two types of poor immunological responder showing distinct responses to long-term HAART.

OBJECTIVES: Most previous studies on poor immunological responders (PIRs) have been performed on one cohort at one time-point following highly active antiretroviral therapy (HAART). The aim of this study was to investigate whether there are different subtypes of PIR and whether a certain population might achieve better immune reconstitution following longer HAART. METHODS: This study was designed as an ambispective cohort study, including a 4-5-year retrospective study and a 2-year prospective follow-up investigation. Thymic output, activated T cell and regulatory T cell (Treg) subset frequencies, expression levels of interferon-stimulated genes, and plasma concentrations of neopterin were determined at 4-5 years and 6-7 years following HAART initiation. RESULTS: PIRs were subdivided into two populations after 4-5 years of HAART, according to the kinetics of T cell recovery. Type II PIRs exhibited a significantly lower percentage of naïve CD4+ T cells and CD31+ naïve CD4+ T cells compared with type I PIRs. After an additional 2 years of HAART treatment, type I PIRs showed a better outcome than type II PIRs. Furthermore, it was found that 2 years of additional HAART could persistently improve thymic output. CONCLUSIONS: The two PIR subgroups are different in terms of immune characteristics and the response to prolonged HAART.

Anemia in combined antiretroviral treatment-naive HIV-infected patients in China: A retrospective study of prevalence, risk factors, and mortality.

Anemia is one of the most important complications of HIV infection. In China, the prevalence, risk factors, and association between anemia and prognosis in HIV-infected patients are poorly elucidated. We analyzed data from 3452 HIV-infected patients not yet on combined antiretroviral therapy (cART) attending Beijing Ditan Hospital from June, 2003 to December, 2015. The overall prevalence of anemia was 9.8% (7.6% mild, 1.9% moderate, and 0.2% severe anemia). Female sex (odds ratio [OR] = 3.71, 95% confidence interval [CI]: 1.46-6.51, p = 0.003), age 40-59 years (OR = 2.54, 95% CI: 1.59-4.05, p < 0.001), body mass index < 18.5 kg/m2 (OR = 2.23, 95% CI: 1.31-3.79, p = 0.003), baseline HIV RNA CI: 1.32-5.99, p = 0.007) were risk factors for anemia. Age 40-59 years (adjusted hazard ratio [AHR] = 5.76, 95% CI: 1.62-20.55, p = 0.007), and anemia ‒ mild (AHR = 7.46, 95% CI: 1.48-37.50, p = 0.015), moderate (AHR = 9.89, CI: 1.35-72.38, p = 0.024), and severe (AHR = 28.29, 95% CI: 2.75-290.54, p = 0.005) anemia ‒ were associated with an increased hazard of death. In this cohort, mild anemia was most common. Anemia was associated with female sex, older age, lower body mass index, lower baseline CD4 count, and higher viral load. Moreover, anemia was associated with an increased risk of death. These findings should promote awareness among physicians to make a timely diagnosis of HIV and to help physicians prioritize prevention and intervention strategies for anemia in HIV-infected patients.

Distinct Mitochondrial Disturbance in CD4+T and CD8+T Cells From HIV-Infected Patients.

BACKGROUND: Mitochondrial dysfunction has frequently been found in HIV-infected patients regardless of whether they received antiretroviral therapy (ART). Accumulating evidence suggests that HIV-infected patients exhibit marked changes in mitochondrial membrane potential (MMP), reactive oxygen species (ROS) accumulation, adenosine triphosphate generation, mitochondrial mass (MM), mitochondrial DNA, etc. However, mitochondrial toxicity in CD4T and CD8T cells caused by different levels of HIV progression and ART is poorly understood. METHODS: Blood samples were obtained from 97 ART-naïve HIV-infected patients with different CD4T cell counts, 97 nucleoside-reverse transcriptase inhibitors-exposed HIV-infected patients, and 25 HIV-negative subjects. MMP, ROS, and MM in CD4T and CD8T cells were assessed by flow cytometry. RESULTS: In healthy subjects, the levels of MMP and MM in CD4T cells were higher than those in CD8T cells. HIV infection led to an increase in MM in CD4T and CD8T cells, but mainly influenced MMP in CD8T cells and ROS accumulation in CD4T cells. MM in CD4T and CD8T cells gradually increased after the loss of CD4T cells. Although the dynamic changes in MMP in CD4T cells were different from those in CD8T cells during highly active ART, MM in both CD4T and CD8T cells was significantly decreased after 2 years of therapy, but increased again after 3 years. CONCLUSIONS: HIV infection and antiretroviral therapy both led to mitochondrial disturbances in CD4T cells and CD8T cells; however, the abnormal changes in mitochondrial parameters in CD4+T cells were different from those in CD8T cells caused by HIV infection and antiretroviral therapy.