Update on the virologic and immunologic response to highly active antiretroviral therapy

Jacobson, Lisa P.; Phair, John P.; Yamashita, Traci E.

doi:10.1007/s11908-004-0055-9

Cited by 9 publications

(12 citation statements)

References 50 publications

(23 reference statements)

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“…CD4 counts started to increase before HIV virus was completely suppressed (time point 0). This is consistent with findings from other studies, that is, CD4 cells may increase after HAART for patients who do not fully suppress the virus, because the level of viral load is decreasing [Jacobson, Phair and Yamashita (2004)]. However, Figure 6(a), also suggests that the decreasing trend for HCV-negative patients ends earlier than HCV-positive patients when HAART started to be initiated.…”

Section: Population Estimatessupporting

confidence: 91%

“…HIV dynamics following initiation of antiviral therapy. The widespread use of highly active antiretroviral therapies (HAART) against HIV in the United States has resulted in reducing the burden of HIV-related morbidity and mortality [Jacobson, Phair and Yamashita (2004)]. HIV dynamics following HAART are usually studied in short-term clinical trials with frequent data collection design.…”

Section: Introductionmentioning

confidence: 99%

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HIV dynamics and natural history studies: Joint modeling with doubly interval-censored event time and infrequent longitudinal data

Su¹,

Hogan²

2011

Ann. Appl. Stat.

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Hepatitis C virus (HCV) coinfection has become one of the most challenging clinical situations to manage in HIV-infected patients. Recently the effect of HCV coinfection on HIV dynamics following initiation of highly active antiretroviral therapy (HAART) has drawn considerable attention. Post-HAART HIV dynamics are commonly studied in short-term clinical trials with frequent data collection design. For example, the elimination process of plasma virus during treatment is closely monitored with daily assessments in viral dynamics studies of AIDS clinical trials. In this article instead we use infrequent cohort data from long-term natural history studies and develop a model for characterizing post-HAART HIV dynamics and their associations with HCV coinfection. Specifically, we propose a joint model for doubly interval-censored data for the time between HAART initiation and viral suppression, and the longitudinal CD4 count measurements relative to the viral suppression. Inference is accomplished using a fully Bayesian approach. Doubly interval-censored data are modeled semiparametrically by Dirichlet process priors and Bayesian penalized splines are used for modeling population-level and individual-level mean CD4 count profiles. We use the proposed methods and data from the HIV Epidemiology Research Study (HERS) to investigate the effect of HCV coinfection on the response to HAART.

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Section: Population Estimatessupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

HIV dynamics and natural history studies: Joint modeling with doubly interval-censored event time and infrequent longitudinal data

Su¹,

Hogan²

2011

Ann. Appl. Stat.

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“…MACS design and methods have been described previously (22–24). In brief, at each semiannual study visit, participants complete a standardized questionnaire soliciting information about their medical history, HIV treatment, behaviors, depression and daily activities, undergo physical examinations and have blood and urine specimens collected for laboratory testing and storage (25). Study questionnaires are available at http://aidscohortstudy.org/.…”

Section: Methodsmentioning

confidence: 99%

An increased rate of fracture occurs a decade earlier in HIV+ compared with HIV− men

Gonciulea

Wang

Althoff

et al. 2017

Aids

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Objectives To determine the incidence and age-related fracture risk among HIV-infected (HIV+) and uninfected men (HIV−). To evaluate factors independently associated with fracture risk. Design Prospective, multicenter cohort study of men with or at risk for HIV. Methods Outcome measures: 1) all fractures (excluding skull, face, digits) and 2) fragility fractures (vertebral column, femur, wrist, humerus) were collected semiannually in 1221 HIV+ and 1408 HIV− men ≥ age 40. Adjusted incident rate ratios (aIRR) with an interaction term for age (40–49, 50–59, ≥60 years) and HIV serostatus were estimated with Poisson regression models accounting for additional risk factors. Results Fracture incidence increased with age among both HIV+ and HIV− men. While there was no significant difference in fracture incidence by HIV serostatus among men aged 40–49 years, the HIV+ men aged 50–59 years had a significantly higher incidence of all fractures (aIRR=2.06 [1.49, 2.84]) and fragility fractures (aIRR=2.06 [1.21, 3.50]) compared with HIV− participants of similar age. HIV modified the effect of age on all fractures (p=0.002) but did not significantly modify the effect for fragility fractures (p=0.135). Hypertension increased the rate of all fractures by 32% after adjustment for covariates (aIRR=1.32 [1.04, 1.69]). Conclusions Fracture incidence increased with age among HIV+ and HIV− men but was higher among HIV+ men. A significant increase in fracture incidence was found among 50–59-year-old HIV+ men, highlighting the importance of osteoporosis screening for HIV infected men above the age of 50.

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“…Study participants returned every 6 months for study evaluations that include a standardized interview, physical examinations, questionnaires (including SF-36 45 and items of the Centers for Epidemiologic Studies Depression Scale (CES-D) 46), and collection of blood for laboratory testing and storage in local and national repositories 47. T-lymphocyte subsets were measured at each MACS center using a standardized flow cytometry protocol.…”

Section: Methodsmentioning

confidence: 99%

Relationship Between a Frailty-Related Phenotype and Progressive Deterioration of the Immune System in HIV-Infected Men

Desquilbet

Margolick

Fried

et al. 2009

JAIDS Journal of Acquired Immune Deficiency Syndromes

152

137

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Context Immunological similarities have been noted between HIV-infected individuals and older HIV-negative adults. Immunologic alterations with aging have been noted in frailty in older adults, a clinical syndrome of high risk for mortality and other adverse outcomes. Using a frailty-related phenotype (FRP), we investigated in the Multicenter AIDS Cohort Study (MACS) whether progressive deterioration of the immune system among HIV positive individuals independently predicts onset of FRP. Methods FRP was evaluated semiannually in 1,046 HIV-infected men from 1994–2005. CD4 T-cell count and plasma viral load were evaluated as predictors of FRP by logistic regression (GEE), adjusting for age, ethnicity, educational level, AIDS status, and treatment era (pre-HAART (1994–1995) and HAART (1996–1999 and 2000–2005)). Results Adjusted prevalences of FRP remained low for CD4 T-cell counts >400 cells/mm3 and increased exponentially and significantly for lower counts. Results were unaffected by treatment era. After 1996, CD4 cell T-count, but not plasma viral load, was independently associated with FRP. Conclusion CD4 T-cell count predicted the development of a frailty-related phenotype among HIV infected men, independent of HAART use. This suggests that compromise of the immune system in HIV-infected individuals contributes to the systemic physiologic dysfunction of frailty.

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Update on the virologic and immunologic response to highly active antiretroviral therapy

Cited by 9 publications

References 50 publications

HIV dynamics and natural history studies: Joint modeling with doubly interval-censored event time and infrequent longitudinal data

HIV dynamics and natural history studies: Joint modeling with doubly interval-censored event time and infrequent longitudinal data

An increased rate of fracture occurs a decade earlier in HIV+ compared with HIV− men

Relationship Between a Frailty-Related Phenotype and Progressive Deterioration of the Immune System in HIV-Infected Men

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