Limited Immune Reconstitution at Intermediate Stages of HIV-1 Infection During One Year of Highly Active Antiretroviral Therapy in Antiretroviral-Naive Versus Non-Naive Adults

2001 ◽  
Vol 20 (12) ◽  
pp. 871-879 ◽  
Author(s):  
M. Martín ◽  
S. Echevarría ◽  
F. Leyva-Cobián ◽  
I. Pereda ◽  
M. López-Hoyos
Keyword(s):  
Antiretroviral Therapy ◽  
Highly Active Antiretroviral Therapy ◽  
Immune Reconstitution ◽  
Highly Active ◽  
One Year ◽  
Hiv 1

Proviral HIV-1 DNA in subjects followed since primary HIV-1 infection who suppress plasma viral load after one year of highly active antiretroviral therapy

AIDS ◽  
2001 ◽  
Vol 15 (6) ◽  
pp. 665-673 ◽  
Author(s):  
Nicole Ngo-Giang-Huong ◽  
Christiane Deveau ◽  
Isabelle Da Silva ◽  
Isabelle Pellegrin ◽  
Alain Venet ◽  
...  
Keyword(s):  
Viral Load ◽  
Antiretroviral Therapy ◽  
Highly Active Antiretroviral Therapy ◽  
Plasma Viral Load ◽  
Highly Active ◽  
One Year ◽  
Hiv 1

Immune reconstitution under antiretroviral therapy: the new challenge in HIV-1 infection

Blood ◽  
2011 ◽  
Vol 117 (21) ◽  
pp. 5582-5590 ◽  
Author(s):  
Pierre Corbeau ◽  
Jacques Reynes
Keyword(s):  
Antiretroviral Therapy ◽  
Highly Active Antiretroviral Therapy ◽  
Immune Reconstitution ◽  
Therapeutic Strategies ◽  
Response To Treatment ◽  
Immune Restoration ◽  
Hiv Replication ◽  
Highly Active ◽  
Hiv 1 ◽  
Etiologic Diagnosis

AbstractAlthough highly active antiretroviral therapy has enabled constant progress in reducing HIV-1 replication, in some patients who are “aviremic” during treatment, the problem of insufficient immune restoration remains, and this exposes them to the risk of immune deficiency–associated pathologies. Various mechanisms may combine and account for this impaired immunologic response to treatment. A first possible mechanism is immune activation, which may be because of residual HIV production, microbial translocation, co-infections, immunosenescence, or lymphopenia per se. A second mechanism is ongoing HIV replication. Finally, deficient thymus output, sex, and genetic polymorphism influencing apoptosis may impair immune reconstitution. In this review we will discuss the tools at our disposal to identify the various mechanisms at work in a given patient and the specific therapeutic strategies we could propose based on this etiologic diagnosis.

scholarly journals Low‐Level Viremia and Proviral DNA Impede Immune Reconstitution in HIV‐1–Infected Patients Receiving Highly Active Antiretroviral Therapy

2005 ◽  
Vol 191 (3) ◽  
pp. 348-357 ◽  
Author(s):  
Sisse R. Ostrowski ◽  
Terese L. Katzenstein ◽  
Per T. Thim ◽  
Bente K. Pedersen ◽  
Jan Gerstoft ◽  
...  
Keyword(s):  
Antiretroviral Therapy ◽  
Highly Active Antiretroviral Therapy ◽  
Immune Reconstitution ◽  
Low Level ◽  
Proviral Dna ◽  
Highly Active ◽  
Hiv 1

T-cell repopulation and thymic volume in HIV-1–infected adult patients after highly active antiretroviral therapy

Blood ◽  
2002 ◽  
Vol 99 (10) ◽  
pp. 3702-3706 ◽  
Author(s):  
Jaime M. Franco ◽  
Amalia Rubio ◽  
Manuel Martı́nez-Moya ◽  
Manuel Leal ◽  
Elena Merchante ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Antiretroviral Therapy ◽  
Highly Active Antiretroviral Therapy ◽  
Immune Reconstitution ◽  
Cell Receptor ◽  
Thymic Tissue ◽  
Highly Active ◽  
Computed Tomography Scanning ◽  
Hiv 1

The origin of T cells after highly active antiretroviral therapy (HAART) in patients infected with human immunodeficiency virus 1 (HIV-1) is now under discussion. The possibility of renewed lymphopoiesis in aged thymuses is still controversial. In this work we combine the analysis of naı̈ve T cells, T-cell receptor excision circles (TRECs), and computed tomography scanning of thymic tissue to further assess whether the thymus is involved in immune reconstitution. Fifteen antiretroviral-naı̈ve HIV-1–infected patients were evaluated during 48 weeks of HAART. At baseline, significant correlation was present among age and both thymic volume and TRECs, and between naı̈ve T cells and TRECs. After starting HAART, there was a significant increase at week 12 in naı̈ve CD4+and CD8+ T cells, TRECs, and thymic volume. The initial net increases in naı̈ve T cells and TREC counts were significantly correlated. Changes in thymic volume and TRECs were also indirectly related; splitting the population into 2 groups of high and low baseline TREC levels, only the group with low TREC levels had significant increases in both TRECs and thymic volume. Thus, the increase in thymic volume might be functional, in response to depleted TREC levels. Taken together, our data strongly suggest a thymic role in immune reconstitution, at least in patients with depleted baseline TREC levels.

HIV-Related Hodgkin Lymphoma in the Era of Highly Active Antiretroviral Therapy: Incidence and Survival in a Prospective European Multi-Cohort Study On Behalf of the Collaboration of Observational HIV Epidemiological Research in Europe (COHERE) Study Group.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 895-895
Author(s):  
Julia Bohlius ◽  
Francois Boue
Keyword(s):  
Antiretroviral Therapy ◽  
Highly Active Antiretroviral Therapy ◽  
Incidence Rates ◽  
Cd4 Cell Count ◽  
Highly Active ◽  
Kaplan Meier ◽  
One Year ◽  
Cd4 Cell ◽  
Hiv 1

Abstract Abstract 895 Introduction: HIV-infected patients are at increased risk to develop Hodgkin Lymphoma (HL). We examined the incidence and risk factors for HL, and the prognosis of patients with HIV-related HL in the era of highly active antiretroviral therapy (HAART) in the Collaboration of Observational HIV Epidemiological Research Europe (COHERE). Patients and Methods: 40,168 adult HIV-1 infected patients who started HAART in one of 16 prospective cohort studies in Europe were included in the present analysis. Incidence rates per 100,000 person-years, Kaplan-Meier estimates of cumulative incidence and survival, and adjusted hazard ratios (HRs) from Weibull random-effects models, with 95% confidence intervals (CIs), were calculated. Results: During 159,133 person-years of follow-up, 78 patients were diagnosed with HL. The crude incidence rate of HL was 50.4 per 100,000 person-years for patients who developed HL before starting HAART (17 cases) and 48.7 per 100,000 person-years in patients who were already on HAART (61 cases). Age, gender, CDC clinical stage, CD4 cell counts and HIV-1 RNA viral load at baseline (start of observation) were not significantly associated with the risk of HL. At HL diagnosis median age was 38.9 years (inter quartile range (IQR) 35.3 - 45.9 years) and the median CD4 cell count was 158 cells/μL (IQR 54 – 281 cells/μL). During a median follow-up of 18 months (IQR 4.8 - 34.8 months) 12 of 78 patients with HL died (15%), six of them during the first 6 months after diagnosis. Survival was 88% (95% CI 77% - 94%) at one year and 81% (95% CI 68% - 89%) at two years. Restricting the analysis to patients aged 16-44 years, one year survival in our population (86%, 95% CI 73% - 93%) was less compared to a European population of male Hodgkin patients of similar age (97.7%) [1]. The figure shows Kaplan-Meier plots of cumulative incidence (upper panel) and survival (lower panel). Conclusions: HL incidence rates were similar in HAART treated and untreated patients. In contrast to HIV-related Non-Hodgkin's Lymphoma no clear association with baseline CD4 cell count was observed. Disclosures: No relevant conflicts of interest to declare.

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