youth ages 18–24 years with baseline CD4 + T-cells >350 who maintained viral suppression on therapy by week 48 were included. Human immunodeficiency virus (HIV) infection is associated with chronic immune activation, and concurrent sexually transmitted infections (STIs) may increase immune activation.īecause HIV-infected youth are at high risk of STIs and little is known about the impact of STIs on immune activation in HIV-infected youth, we conducted an exploratory study examining the association between STIs and systemic inflammation and immune activation among HIV-infected adolescents.įorty-nine behaviorally infected U.S. Overall, these findings indicate that mTOR inhibitors constrain the inflammation/immune activation and senescence status, thus reducing the expansion of EBV-infected B cells and the risk of virus-associated PTLD in kidney transplant recipients. Percentages of activated B cells and levels of EBV-DNA significantly increased in MPA-treated patients, and at T1 were significantly higher in MPA- than in mTORi-treated patients. At the time of the transplant (T0), profile of inflammation/immune activation and immune senescence didn't differ between the two groups, but after one year of treatment (T1) markers were significantly higher in MPA-treated patients their immunosenescence process was supported by the greater erosion of telomeres despite their younger age. 124 kidney transplanted patients were enrolled in this study: 71 were treated with mycophenolic acid (MPA) and 53 treated with mTOR inhibitor (mTORi), both in combination with different doses of calcineurin inhibitor. The aim of this study was to assess the impact of immunosuppressive strategies on factors involved in the PTLD's pathogenesis. Besides immunodepression, immune activation/chronic inflammation play an important role in both virus reactivation and expansion of EBV-positive B cells. Post-transplant lymphoproliferative disorders (PTLD) represent a severe complication in transplanted patients and Epstein-Barr Virus (EBV) is the main driver. We thank Lisa Smith for editorial assistance and Pierantonio Gallo for the artwork. Persistence of plasma viremia during HAART, despite immunoreconstitution, is not an infrequent observation,16, 20, 24, 25, Acknowledgment 15 Chronic immune activation is a hallmark of HIV-1 infection and may contribute to the expansion of EBV-infected cells.
Only 17 naïve patients had severe immunodepression (CD4 < 200 cells/μl), whereas 52 (73%) naïve, 21 (33%) Discussionįollowing the introduction of HAART, the incidence of opportunistic infections and AIDS-related diseases, such as Kaposi sarcoma, dramatically decreased.22, 23 However, the impact of HAART in preventing EBV-associated lymphomas seems to be less effective.
EBV-DNA levels were higher in naïve and out of therapy patients than in those in HAART (overall, p = 0.001) (Table 1).ĬD4 cell number was lower in naïve patients and in those out of therapy than in HAART patients (overall, p < 0.0001) (Table 1). The median EBV-DNA load was 43 copies/10 5 PBMC. Patients were treated according to current guidelines for HIV-1 infection.17, 18 Among EBV-DNA levels in relationship to CD4 cell count and HIV-1 loadĮBV-DNA was detected in 114 patients in all but 3 cases EBV was type 1. At the time of sample collection for the study, 71 (45%) were HAART-naïve, and 85 (55%) HAART-experienced with a median (range) of 6 (1–10) years of HAART. Their median age was 41 (range 18–68) years. Patients and samplesĪ total of 156 (117 male and 39 female) HIV-1-infected patients who attended the Infectious Diseases Division of Rovigo Hospital consecutively from July 2007 to December 2009 were included in this study. The aim of this study was to investigate the relationship between HIV-1 viremia, markers of immune activation and EBV load in HIV-1 infected HAART-naïve and HAART-experienced patients. 1 Patients with HIV-1 infection are at high risk of developing EBV-related diseases, ranging from lymphoproliferatives disorders to B-cell non-Hodgkin's lymphomas (NHL).2, 3īesides immunodepression, chronic immune activation, a hallmark of HIV-1 pathogenesis, 4 may play a critical role in the genesis of B-cell lymphomas.5, 6 Cell activation driven Objectives EBV infects B lymphocytes and has a potent transforming ability, capable of inducing uncontrolled proliferation and transformation of infected cells.
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